By Carl E. Stafstrom, Jong M. Rho
A benchmark synthesis of the present nation of the technology and medical perform of the ketogenic nutrition. at the easy technological know-how facet, the authors evaluate what's identified in regards to the simple biochemical mechanisms of motion of the KD on the molecular point, spelling out intimately its advanced interactions with nutrient parts, neurodevelopment, mind biochemistry, and body structure. additionally they learn the results of the KD at the metabolism of fat, amino acids, and carbohydrates within the significant worried procedure at either the macro and mobile degrees. at the scientific part, physicians, dietitians, and nurses offer a whole variety of knowledge about the remedy of seizures with KD, together with a close overview of the indicators for, and the contraindications and/or problems that come up from, its use, specified equations that let the caregiver to calculate the particular quantities of other different types of meals that may be incorporated in day-by-day nutrition plans, and documented details at the carbohydrate and calorie content material of thousands of commonplace medicinal drugs.
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Extra info for Epilepsy and the Ketogenic Diet: Clinical Implementation & the Scientific Basis (Nutrition and Health)
The lowermost traces, recordings from neuron 2, show activity similar to that recorded in neuron 1, occurring a bit later owing to a synaptic delay (double-headed horizontal arrow). Activation of inhibitory neuron 3 by ﬁring of neuron 1 prevents neuron 2 from generating an action potential (the IPSP counters the depolarization caused by the EPSP). ). (Modiﬁed with permission of the American Academy of Pediatrics from ref. ) Chapter 1 / Seizures and Epilepsy 19 huge number of neurons is ﬁring synchronously, the result of which would be a clinical seizure with manifestations correlating with the area of brain involved.
Baram TZ, Hatalski CG. Neuropeptide-mediated excitability: a key triggering mechanism in the developing brain. Trends Neurosci 1998;21:471–476. 23. Vezzani A, Sperk G, Colmers WF. Neuropeptide Y: emerging evidence for a functional role in seizure modulation. Trends Neurosci 1999;22:25–30. 24. Colmers WF, Bahh BE. Neuropeptide Y and epilepsy. Epilepsy Curr 2003;3:53–58. 25. Wasterlain CG, Mazarati AM. Neuromodulators and second messengers. ). Epilepsy: A Comprehensive Textbook. Lippincott-Raven, Philadelphia, PA, 1997, pp.
Another new AED, tiagabine (TGB), also increases GABA availability but by a different mechanism: preventing GABA reuptake into the presynaptic terminal. The mechanism of action of gabapentin (GBP), despite the presence of GABA in its name, is still unresolved; GBP may increase the rate of GABA synthesis or release. Other AEDs affect aspects of neuronal excitation. Phenytoin and carbamazepine, and the newer AEDs lamotrigine and zonisamide, block voltage-dependent sodium channels and reduce the ability of neurons to ﬁre repetitively.
Epilepsy and the Ketogenic Diet: Clinical Implementation & the Scientific Basis (Nutrition and Health) by Carl E. Stafstrom, Jong M. Rho