Causes and consequences of pathogenic processes in evolution: implications from experimental epilepsy in animals
ABSTRACT Examples from experimental epilepsy in animals are used to illustrate the view that a crucial role of the transfer of mechanisms from compensatory into pathogenic (e.g. lethal ones in the course of a disease), is played by the power of pathologic stimuli. In the genesis of epilepsy it is suggested that a critical increase of endogenous factors may underlie the conversion of the absence form of epilepsy into a generalized self-supporting form. The ability to precipitate endogenous self-augmenting mechanisms of diseases may have increased in the course of evolution. The lethal result of a serious pathogenic process leads to the suggestion that organisms cope with the disease by dying. This prevents spreading of the putative infectious disease within the population. This mechanism of disease aggravation could play a role in the survival of the species and in further evolutionary progress. This may explain why certain species may have survived in evolution and supports the theory of synthetic evolution.
SourceAvailable from: Olivera Stanojlovic
Article: [Experimental models of epilepsy].[Show abstract] [Hide abstract]
ABSTRACT: An epileptic seizure is a clinical event and epilepsy is rather a group of symptoms than a disease. The main features all epilepsies have in common include, spontaneous occurrence, repetitiveness, and ictal correlation within the EEG. Epilepsies are manifested with distinct EEG changes, requiring exact clinical definition and consequential treatment. Current data show that 1% of the world's population (approximately 50 million people) suffers from epilepsy, with 25% of patients bpeing refractory to therapy and requiring search for new substances in order to decrease EEG and behavioral manifestations of epilepsies. In regard to discovery and testing of anticonvulsant substances the best results were achieved by implementation of experimental models. Animal models of epilepsy are useful in acquiring basic knowledge regarding pathogenesis, neurotransmitters (glutamate), receptors (NMDA/AIPA/kainate), propagation of epileptic seizures and preclinical assessment of antiepileptics (competitive and non-competitive NMDA antagonists). In our lab, we have developed a pharmacologic model of a (metaphit, NMDA and remacemide-cilastatin) generalized, reflex, and audiogenic epilepsy. The model is suitable for testing various anticonvulsant substances (e.g. APH, A4P, CPP, Mk-801) and potential antiepileptics (e.g. DSIP, its tetra- and octaanalogues).Medicinski pregled 01/2004; 57(7-8):359-62. DOI:10.2298/MPNS0408359S