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The Medical Use of Marijuana in Epilepsy
Cannabinoids have been used to treat epilepsy patients since Sumerian healers prescribed it in 1800 B.C.E. English and American neurologists used cannabis (marijuana) to treat epilepsy and reported selected cases with marked reductions in seizure frequency. The isolation and synthesis of cannabidiol (CBD) and Δ9-tetrahydrocannibinol (THC) by Dr. Raphael Mechoulam’s group led to an interest in the neuropharmacology of these compounds and their potential uses. Four trials of CBD for epilepsy in the 1970s produced mixed results, but two of these studies suggested that CBD might be effective for epilepsy. Although many patients anecdotally report that cannabis can improve seizure control, there was little systematic study of cannabis therapies for epilepsy until 2012, when media reports sparked renewed interest. During the past several years, an increasing number of US states have approved medical cannabis (or the constituents of cannabis) to treat various disorders, including epilepsy.
This module will review the available research and clinical evidence for the use of cannabis in the treatment of epilepsy.
The endocannabinoid system is activated by seizures. Further, increasing CB1 receptor activity has anti-seizure effects (1). In mice given systemic kainic acid to induce seizures, hippocampal anandamide levels rise after seizures. When neurons cultured from the hippocampus are exposed to CB1 receptor antagonists, prolonged seizure discharges are produced (2); these discharges are suppressed by CB1 receptor agonists (3). Drugs that reduce the metabolism of endocannabinoids and thereby increase their activity, help to control experimentally induced seizures (4).
Yes. There are defects in the endocannabinoid system in persons with epilepsy. In one study, 12 patients with newly diagnosed temporal lobe epilepsy had lower levels (p < .01) of anandamide in spinal fluid as compared to controls (5). In tissue removed from 30 patients undergoing epilepsy surgery, the levels of CB1 receptor messenger RNA were lower in some excitatory nerve endings as compared to the specimens obtained post mortem from persons without epilepsy. It was also noted that in the epilepsy patients, there was reduced expression of diacylglycerol lipase α (DAGL-α), the enzyme that synthesizes 2-AG in postsynaptic neurons (6). (Recall that 2-AG is a fully efficacious agonist of both CB1 and CB2 receptors.)