By Carl E. Stafstrom, Jong M. Rho
A benchmark synthesis of the present kingdom of the technology and scientific perform of the ketogenic nutrition. at the simple technology aspect, the authors overview what's recognized concerning the easy biochemical mechanisms of motion of the KD on the molecular point, spelling out intimately its complicated interactions with nutrient elements, neurodevelopment, mind biochemistry, and body structure. in addition they study the results of the KD at the metabolism of fat, amino acids, and carbohydrates within the critical fearful process at either the macro and mobile degrees. at the scientific part, physicians, dietitians, and nurses offer a whole diversity of knowledge in regards to the remedy of seizures with KD, together with an in depth evaluate of the symptoms 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 kinds of meals that may be integrated in day-by-day nutrition plans, and documented info at the carbohydrate and calorie content material of countless numbers of normal medicines.
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Extra resources for Epilepsy and the Ketogenic Diet: Clinical Implementation & the Scientific Basis (Nutrition and Health)
Dunwiddie TV, Masino SA. The role and regulation of adenosine in the central nervous system. Annu Rev Neurosci 2001;24:31–55. 33. Schwartzkroin PA. Basic mechanisms of epileptogenesis. ) The Treatment of Epilepsy: Principles and Practice. Lea & Fibiger, Philadelphia, 1993, pp. 83–98. 34. McCormick DA, Contreras D. On the cellular and network bases of epileptic seizures. Annu Rev Physiol 2001;63:815–846. 35. Clark S, Wilson WA. Mechanisms of epileptogenesis. Adv Neurol 1999;79:607–630. 36. Sarkisian MR.
The PDS is initiated or “kicked off” by a fast, non-NMDA-mediated EPSP and sustained by a prolonged, NMDA-mediated EPSP. Compared with the usual NMDA-mediated slow EPSP of approx 10–20 ms, the PDS is longer (30–50 ms) with many more action potentials on top of the depolarization. ). The PDS is followed by a large “post-PDS hyperpolarization” (asterisk in Fig. 5B), which serves to terminate the PDS and stop, at least temporarily, the rampant ﬁring of action potentials. Note that a PDS in neuron 1 may activate a similar PDS in neuron 2, and so on, such that a whole network of neurons can be rapidly recruited into ﬁring in a synchronous manner.
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. 277–289. 26. Binder DK, Croll SD, Gall CM, Scharfman HE. BDNF and epilepsy: too much of a good thing? Trends Neurosci 2001;24:47–53. 27. Maragakis NJ, Rothstein JD. Glutamate transporters in neurologic disease. Arch Neurol 2001;58:365–370. 28. Raiteri L, Raiteri M, Bonanno G.