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Review
. 2015 Oct;4(4):271-82.
doi: 10.3978/j.issn.2224-4336.2015.10.03.

Cannabinoids for pediatric epilepsy? Up in smoke or real science?

Francis M Filloux  1
Affiliations
Review

Cannabinoids for pediatric epilepsy? Up in smoke or real science?

Francis M Filloux. Transl Pediatr. 2015 Oct.

Abstract

Public interest in the use of "medical marijuana" for the treatment of childhood epilepsy has burgeoned in the last few years. This has occurred in parallel with a growing interest in "medical marijuana" in general. Physicians and pediatricians must balance their patients' desire for immediate access to these products with the tenets of evidence-based medicine. This review discusses the biochemistry of cannabis products (the phytocannabinoids) setting this in the context of the endogenous endocannabinoid system. The differing and potentially modulating effects of delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) are reviewed. The evidence-base supporting or not the use of cannabis products for the treatment of neurological disease and specifically epilepsy is explored. The potential for adverse effects and particularly of neurotoxicity is addressed. Finally, public health and sociocultural implications are touched upon. Specific recommendations for interested physicians are provided including advocacy for patients and for a change in the "scheduling" of cannabis in order to better foster much-needed high-quality scientific research in this important area.

Keywords: Cannabidiol (CBD); cannabis; epilepsy; medical marijuana; tetrahydrocannabinol (THC).

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Conflict of interest statement

Conflicts of Interest: The author has no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Terpene phenolic heterocyclic structures of delta-9-tetrahydrocannabinol (THC) and cannabidiol (CBD). Red portions identify basic terpene (left) and phenol (right) backbones.
Figure 2
Figure 2
Schematic of a GABAergic synapse modulated by CB1 receptors. The perisynaptic location of CB1 receptors (A) is depicted. GABA (E) stimulates post-synatpic GABA receptors (F). Post synaptic changes induce metabolism of membrane derived phospholipids (G) leading to formation of endocannabinoid (H). The latter diffuses back stimulating the perisynaptic CB1 receptor (A). This in turn modulates neurotransmitter release from presynaptic vesicles (D) via G-protein coupled (B) influence on Ca++ channels (C).
Figure 3
Figure 3
Chemical structures of the two major endocannabinoids: N-arachidonyl ethanolamide (AEA; “anandamide”) and 2 arachidonoylglycerol (2AG). Similarity to arachidonic acid and arachidonic acid metabolites is apparent.
Figure 4
Figure 4
Comparison of Pharmaceutical Grade Cannabidiol (CBD) vs. Vernacular Preparations (“hemp-oil”). THC, tetrahydrocannabinol.
See this image and copyright information in PMC

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