Читать книгу Canine and Feline Epilepsy - Luisa De Risio - Страница 35

Although the functions of many inflammatory mediators remain unresolved, clear evidence exists for an active role for IL-1β, TNF, IL-6, prostaglandin E2 (PGE2) and the complement cascade in seizure generation and exacerbation (Xiong et al., 2003). Seizure activity leads to the production of inflammatory molecules that, in turn, affect seizure severity and recurrence, and this action takes place through mechanisms distinct from the transcriptional events traditionally activated during systemic inflammation. Cerebrospinal fluid studies in children and animal models have implicated the release of endogenous cytokines, especially IL-1β, in the generation of febrile seizures and, possibly, in the development of epilepsy after febrile seizures (Haspolat et al., 2002; Virta et al., 2002; Dube et al., 2005; Heida and Pittman, 2005; Vezzani et al., 2013).

A positive feedback pathway has been identified in rat models between seizure activity and the presence of inflammation (Vezzani et al., 2011). However, the role of inflammation in epilepsy in veterinary medicine has really only been described clinically in cats with hippocampal necrosis (Fatzer et al., 2000). Hippocampal lesions of 38 cats with seizures have been described and seemed to reflect different stages of disease consisting 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 excitotoxicity, but secondary inflammation cannot be ruled out in these cases.