By David W. McCandless
The current quantity is meant to be a synopsis of seizure problems with a aim of describing key reports in animals and people. the interpretation of pertinent findings from animal reviews to human reviews, and to power human experiences might be emphasised. particular cogent animal studies/results which deserve exploration in human seizure problems should be distinctive. the present cost of translation is anticipated to be from 7‐9 years, and the “success” price of translation was once very lately indexed as lower than one part. The good fortune price is outlined as leads to human reviews which have been envisioned prematurely through animal reviews. either the time among animal and human makes an attempt plus the luck cost desire improvement.
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Additional resources for Epilepsy: Animal and Human Correlations
Data expressed as nmoles/mg dry weight. 005. , et al. Am J. Physiol. 251: p. 0 1 2 3 4 CONTROL 1 2 3 4 SEIZURE 1 2 3 4 RECOVERY Fig. 4 Effect of bicuculline-induced seizures and recovery on regional motor cortex ATP. Layers and significance as in Fig. 3. , et al. Am J. Physiol. 251: p. 01 10 8 6 4 2 CONTROL SEIZURE SHUT DOWN Fig. 5 Hippocampal CA1 phosphocreatine during and after seizure activity. Data (mean plus/minus SEM) expressed as nmoles/mg dry weight. Redrawn from DeFrance, J. and McCandless, D.
Data support evidence for genetic effects on generalized vs. localization-related epilepsy (Winawer et al. 2003). 3 Epidemiology of Epilepsy 37 The authors comment that a thorough history is critical in ascertaining risk for offspring of parents who both have seizures. The etiology of parental epilepsy is important to determine if possible. The overall risk is relatively small except in monozygotic twins. Associated above, juvenile myoclonic epilepsy has an etiologic genetic factor, and the epidemiology has been examined (Welty 2006).
24 2 Metabolism and Epilepsy Posttraumatic epilepsy is a common long latency after effect of TBI. This can occur in both pediatric and adult TBI patients. That the A1 receptor is involved in seizure suppression is shown by results in which an A1 receptor knockout mouse is highly susceptible to status epilepticus. Even in cases in which there are no overt seizures, epileptiform activity is demonstrable. Studies implicate adenosine dysregulation in epileptogenesis (Boison 2008b). A group of inborn errors of creatine metabolism have been recently described (Schulze 2003).