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Review
. 2013 Jun;19(3 Epilepsy):756-66.
doi: 10.1212/01.CON.0000431396.23852.56.

Dietary treatment of intractable epilepsy

Mackenzie C Cervenka  1 , Eric H Kossoff
Affiliations
Review

Dietary treatment of intractable epilepsy

Mackenzie C Cervenka et al. Continuum (Minneap Minn). 2013 Jun.

Abstract

Purpose of review: Dietary therapies for seizure management date back further than pharmacologic interventions, but many neurologists are not familiar with these treatment options. This introduction to dietary therapies will discuss administration of ketogenic diets, comparisons between diet types, evidence-based efficacy of diet therapies in epilepsy treatment, and management of side effects. This review will provide the general neurologist with the skills to identify appropriate candidates for these treatments and to offer comprehensive ongoing care.

Recent findings: In adults and children with medically resistant epilepsy, studies have consistently shown a greater than 50% reduction in seizure frequency in approximately one-half of patients within days to months after starting dietary therapy.

Summary: Dietary treatment options for epilepsy include the classic ketogenic diet, the medium-chain triglyceride diet, the modified Atkins diet, and the low glycemic index treatment. These were first used to control seizures in children with intractable epilepsy, but in recent years have also been demonstrated to be safe and effective in children and adults with a broad range of seizure types and are being used with increased frequency worldwide.

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Figures

Figure 11-1.
Figure 11-1.
Potential antiepileptic mechanisms of action of ketogenic diets. Ketone bodies produced during treatment with ketogenic diets may influence the metabolic pathways of several neurotransmitters including γ-aminobutyric acid (1, 4), glutamate (2, 5), adenosine (3), norepinephrine (3), and the Krebs cycle (6). GABA = γ-aminobutyric acid; GLN = glutamine; GLU = glutamate; ROS = reactive oxygen species; GABABR = γ-aminobutyric acid β receptor; GABAAR = γ-aminobutyric acid α receptor, Cl− = chloride; VGLUT = vesicular glutamate transporter; KATP = potassium adenosine triphosphate; A1R = adenosine receptor. Reprinted with permission from McNally MA, Hartman AL, J Neurochem. © 2012 International Society for Neurochemistry. onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2012.07670.x/abstract.
See this image and copyright information in PMC

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