Treating epilepsy with medical cannabis
Medical cannabis has been found to be effective in reducing the frequency and severity of seizures in patients with epilepsy. Epilepsy is a neurological disorder characterized by recurring seizures or convulsions caused by abnormal electrical activity in the brain. It can be a debilitating condition that affects the quality of life of patients and can be difficult to manage with traditional treatments.
Cannabis contains a range of compounds, including cannabinoids and terpenes, that interact with the body's endocannabinoid system (ECS). The ECS plays a key role in regulating a range of physiological processes, including pain, inflammation, and neurological function.
One of the main cannabinoids found in cannabis is cannabidiol (CBD), which has been shown to have anticonvulsant properties. CBD works by interacting with the body's ECS to modulate the release of neurotransmitters and reduce inflammation, which can contribute to seizures.
Studies have found that CBD can be effective in reducing the frequency and severity of seizures in patients with epilepsy, including those with treatment-resistant forms of the condition. In one study published in the New England Journal of Medicine, researchers found that CBD reduced the frequency of seizures by 39% in patients with Dravet syndrome, a rare and severe form of epilepsy.
Another study published in the Journal of Epilepsy Research found that CBD reduced the frequency of seizures by 50% or more in 70% of patients with treatment-resistant epilepsy. These results suggest that CBD may be a promising treatment option for patients with epilepsy who have not responded to traditional treatments.
While CBD has shown promise in treating epilepsy, it is important to note that not all forms of medical cannabis may be effective for this condition. THC, another major cannabinoid found in cannabis, can actually increase the risk of seizures in some patients.
For this reason, medical cannabis products for epilepsy are often formulated to contain high levels of CBD and low levels of THC. These products are often referred to as "CBD-rich" or "high-CBD" strains.
Medical cannabis products for epilepsy are typically administered orally in the form of oils, capsules, or tinctures. The dosing and frequency of use can vary depending on the patient's individual needs and the severity of their condition.
It is important for patients to work closely with their healthcare provider to determine the most appropriate form of medical cannabis and dosing regimen for their individual needs. They should also be monitored for potential side effects, such as drowsiness, changes in appetite, or interactions with other medications.
In conclusion, medical cannabis has shown promise as a treatment option for patients with epilepsy, particularly those with treatment-resistant forms of the condition. CBD, a major cannabinoid found in cannabis, has been found to have anticonvulsant properties and can be effective in reducing the frequency and severity of seizures. However, it is important to work closely with a healthcare provider to determine the most appropriate form and dosing of medical cannabis for each patient's individual needs.
Research on medical cannabis and its role on treating epilepsy
1. Time to Onset of Cannabidiol (CBD) Treatment Effect and Resolution of Adverse Events in Tuberous Sclerosis Complex: Post Hoc Analysis of Randomized Controlled Phase 3 Trial GWPCARE6
Summary
Objective
To estimate the timing of cannabidiol (CBD) treatment effect (seizure reduction and adverse events [AEs]) onset, we conducted a post hoc analysis of GWPCARE6 (NCT02544763), a randomized, placebo-controlled, phase 3 trial in patients with drug-resistant epilepsy associated with tuberous sclerosis complex (TSC).
Methods
Patients received plant-derived pharmaceutical formulation of highly purified CBD (Epidiolex®; 100 mg/mL oral solution) at 25 mg/kg/day (CBD25) or 50 mg/kg/day (CBD50) or placebo for 16 weeks (4-week titration, 12-week maintenance). Treatment started at 5 mg/kg/day for all groups and reached 25 mg/kg/day on Day 9 and 50 mg/kg/day on Day 29. Percentage change from baseline in TSC-associated seizure (countable focal or generalized) count was calculated by cumulative day (i.e., including all previous days). Time to onset and resolution of AEs were evaluated.
Results
Of 224 patients, 75 were randomized to CBD25, 73 to CBD50, and 76 to placebo. Median (range) age was 11.3 (1.1–56.8) years. Patients had discontinued a median (range) of 4 (0–15) antiseizure medications and were currently taking 3 (0–5). Difference in seizure reduction between CBD and placebo emerged on Day 6 (titrated dose, 15 mg/kg/day) and became nominally significant (p<0.049) by Day 10. Separation between placebo and CBD in ≥50% responder rate also emerged by Day 10. Onset of AEs occurred during the first 2 weeks of the titration period in 61% of patients (CBD25, 61%; CBD50, 67%; placebo, 54%). In patients with an AE, resolution occurred within 4 weeks of onset in 42% of placebo and 27% of CBD patients and by end of trial in 78% of placebo and 51% of CBD patients.
Significance
Onset of treatment effect occurred within 6–10 days. AEs lasted longer for CBD than placebo but the most common (diarrhea, decreased appetite, and somnolence) resolved during the 16-week trial in most patients.
2. Are blood and oral fluid Δ9-tetrahydrocannabinol (THC) and metabolite concentrations related to impairment? A meta-regression analysis
Abstract
Blood and oral fluid Δ9-tetrahydrocannabinol (THC) concentrations are often used to identify cannabis-impaired drivers. We used meta-analytic techniques to characterise the relationships between biomarkers of cannabis use, subjective intoxication, and impairment of driving and driving-related cognitive skills. Twenty-eight publications and 822 driving-related outcomes were reviewed. Each outcome was measured in concert with one or more biomarkers of cannabis/THC use and/or subjective intoxication. Higher blood THC and 11−OH-THC concentrations, oral fluid THC concentrations and subjective ratings of intoxication were associated with greater impairment in ‘other’ (mostly occasional) cannabis users (p’s<0.05). Blood 11−COOH-THC concentrations were associated with impairment after inhaling, but not orally ingesting, cannabis/THC. However, these ‘biomarker–performance’ relationships (R) were only very weak (blood THCpost-ingestion: -0.08; blood THCpost-inhalation: -0.10; blood 11−OH-THCpost-ingestion: -0.13), weak (blood 11−OH-THCpost-inhalation: -0.24; oral fluid THCpost-inhalation: -0.36; subjective intoxication: -0.29) or moderate (blood 11−COOH-THCpost-inhalation: -0.43) in strength. No significant biomarker-performance relationships were observed in ‘regular’ (weekly or more often) cannabis users (p’s>0.10), although the analyses were less robust. Blood and oral fluid THC concentrations are relatively poor indicators of cannabis/THC-induced impairment.