Epilepsy and the Ketogenic Diet: Clinical Implementation & by Carl E. Stafstrom, Jong M. Rho

By Carl E. Stafstrom, Jong M. Rho

A benchmark synthesis of the present kingdom of the technological know-how and scientific perform of the ketogenic vitamin. at the easy technology aspect, the authors assessment 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 elements, neurodevelopment, mind biochemistry, and body structure. additionally they learn the consequences of the KD at the metabolism of fat, amino acids, and carbohydrates within the critical frightened approach at either the macro and mobile degrees. at the medical part, physicians, dietitians, and nurses supply an entire diversity of data in regards to the therapy 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, designated equations that allow the caregiver to calculate the particular quantities of alternative sorts of meals that may be integrated in day-by-day nutrition plans, and documented details at the carbohydrate and calorie content material of 1000s of prevalent medicinal drugs.

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All of these mechanisms vary over different stages of brain development. Rational treatment of epilepsy, whether with anticonvulsant medications, surgical interventions, or the ketogenic diet, requires an understanding of the age-specific physiological features that govern neuronal function. REFERENCES 1. Commission on Classification and Terminology of the International League Against Epilepsy. Proposal for revised clinical and electroencephalographic classification of epileptic seizures. Epilepsia 1981;22:489–501.

This chronic hyperexcitability is a result of the combined effects of several structural alterations: neuronal death, gliosis or mesial temporal sclerosis, and the growth of new, abnormal axonal connections (“sprouting”). Figure 7 depicts how such sprouting might work by producing aberrant excitatory connections. Dentate granule neurons (Fig. 7A, circles 1, 2) receive all incoming activity entering the hippocampus. Ordinarily, dentate neurons fire only single action potentials (right panel, 22 Part I / Background Fig.

2A). Influx of calcium ions (Ca2+) caused by depolarization of the terminal of the inhibitory neuron causes vesicles to release GABA into the synaptic cleft. GABA diffuses across the cleft and binds to its receptors (GABAA), and this sequence opens a pore or channel through which chloride ions (Cl–) enter the neuron. This Cl– influx increases the negative charge inside the postsynaptic neuron, hyperpolarizing it. The resultant change in membrane potential is called an inhibitory postsynaptic potential (IPSP) (Fig.

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