The question of whether cannabis use can provoke a seizure is a significant public health concern, especially given the increased availability of cannabis products. The plant contains over one hundred active chemical compounds, known as cannabinoids, which interact with the central nervous system in complex ways. Understanding the relationship between cannabis and seizure activity requires separating the effects of the plant’s different components, particularly the psychoactive compound versus the non-psychoactive one, as they have opposing effects on brain function.
How THC Affects Seizure Thresholds
The primary psychoactive component in cannabis, delta-9-tetrahydrocannabinol (THC), interacts directly with the brain’s cannabinoid receptor type 1 (CB1). This interaction modulates the release of various neurotransmitters, potentially disrupting the balance between excitatory and inhibitory signals necessary for stable neuronal function. The overall effect of THC on seizure susceptibility is complex and dose-dependent.
Consuming high doses of THC may lower the seizure threshold, making the brain more susceptible to a seizure trigger. This occurs because THC can increase neuronal excitability, sometimes by reducing the inhibitory effects of GABA while enhancing the effects of the excitatory neurotransmitter glutamate. This imbalance shifts the brain toward a state where abnormal electrical firing is more likely to occur.
Interestingly, THC has demonstrated anticonvulsant properties at very low concentrations, illustrating a biphasic effect. Current medical consensus suggests that natural cannabis is an infrequent direct cause of seizures in otherwise healthy people. The risk appears highest when the cannabis has a high concentration of THC and a low concentration of other balancing compounds.
Cannabidiol (CBD) as an Anticonvulsant
The complexity of cannabis is further highlighted by the non-psychoactive compound, Cannabidiol (CBD), which has demonstrated strong anticonvulsant properties, in contrast to THC. Highly purified, pharmaceutical-grade CBD has received regulatory approval for the treatment of specific, severe forms of childhood epilepsy, including Dravet syndrome and Lennox-Gastaut syndrome. This therapeutic use results from CBD operating through mechanisms distinct from the CB1 receptor pathway utilized by THC.
CBD’s anti-seizure effect is multimodal, targeting several different non-cannabinoid receptors and ion channels to reduce excessive neuronal firing. CBD acts as an antagonist at the G protein-coupled receptor 55 (GPR55), which increases neuronal excitability when activated. By inhibiting GPR55, CBD helps decrease excitatory currents and quell seizure activity.
TRPV1 Modulation and Adenosine Reuptake
It also modulates the activity of the transient receptor potential vanilloid type 1 (TRPV1) channels, which regulate calcium influx and neurotransmission. Furthermore, CBD can inhibit the reuptake of adenosine, a neuromodulator that reduces neuronal hyperexcitability, thereby increasing the brain’s natural anti-seizure signaling. This combination of actions allows CBD to dampen the electrical activity that characterizes epileptic seizures without causing the intoxication associated with THC.
Increased Risk Factors: Withdrawal and Synthetic Compounds
While the use of natural cannabis is not a common direct trigger for seizures in the general population, two specific scenarios present a significantly higher risk: synthetic compounds and acute withdrawal.
Synthetic Cannabinoids
Synthetic cannabinoids, often sold illegally as “K2” or “Spice,” are chemically distinct substances that pose danger. These compounds are full agonists of the CB1 receptor, activating the receptor much more powerfully and unpredictably than natural THC. This intense activation can lead to severe and toxic reactions, with seizures being a well-documented adverse effect in otherwise healthy individuals. Their toxicity is substantially greater than that of natural cannabis, and their use requires emergency medical attention.
Acute Withdrawal
The second high-risk factor involves the acute withdrawal experienced by heavy, long-term cannabis users upon cessation. Chronic exposure to THC causes the brain to adapt by reducing the number of available CB1 receptors, a process known as downregulation. When the substance is suddenly removed, the brain is thrown into a state of neurobiological imbalance. Although the most common symptoms of cannabis withdrawal syndrome are mood changes, anxiety, and sleep disturbances, the destabilization of neuronal function increases the risk for seizures in individuals with underlying susceptibility. Seizures are a rare but possible symptom of this withdrawal, reflecting the brain’s difficulty in rapidly adjusting its excitability levels.