Cannabidiol: mechanisms and efficacy in medically refractory epilepsy

Virginia Thornley, M.D., Neurologist, Epileptologist

March 9, 2018


One of the most challenging therapeutic goals are to keep patients with epilepsy seizure free. Once a patient is found to be medically refractory, it is not unusual to find patients on 3-4 medications for seizure control. However, oftentimes, the means to the end is often wrought with its own challenges with patients suffering side effects placing their quality of life secondary to the medical control of their condition. More and more patients and their families are turning towards a more naturalistic approach including diet and cannabidiol use which has fewer side effects as a means to control seizures. The literature is fraught with a paucity of scientific data with small clinical trials, animal models, and anecdotal data. Larger clinical randomized control trials are pursued.


Mechanisms of Cannabidiol and THC

In the brain, there is the natural endocannabinoid system. Endocannabinoids are released after exercise referred to as the runner’s high which contributes towards our sense of well-being. In the endocannabinoid pathway, cannabidiol has a low affinity to the CB1 receptor and modulates THC tetrahydrocannabinol by blocking CB1 receptor. It is thought to modulate THC by blocking the CB1 receptor acting as an inverse CB1 agonist (2). This may be the mechanism behind combining CBD with THC, CBD modulates the side effects of THC making it less available to exert its effects. Delta9THC is found to work at the level of the CB1 receptors which are rich in the brain and CB2 receptor which is more predominant in the immune system. THC can bind to other targets exerting inflammatory properties. CBD has less binding capabilities to CB1 receptors and is thought to exert its effect by working through other mechanisms such as voltage-gated potassium and sodium channels and the GRP55 in controlling seizures. Cannabinoids are lipid binding or lipophilic making it less available within the system making it challenging to deliver (3).

Cannabidiol clinical trials

In one study, 216 patients were enrolled and followed 3 months after administration of the first dose cannabidiol. Initially, the dose was 2mg/kg which was titrated up to 50mg/kg. 76% were enrolled in the safety profile study and 64% were enrolled in the efficacy profile study. In the first group for safety, 20% had Dravet syndrome and 19% had Lennox-Gastaut syndrome. Side effects were noted in 79% of the patients in the safety group. These include somnolence, diarrhea, seizures (11%), fatigue and reduced appetite. Five disenrolled due to adverse effects, 30% had serious side effects including 1 death of consisting sudden death syndrome. 12% had serious side effects including status epilepticus which may have been related to cannabidiol use. The median reduction of seizures was 36.5%. The study concluded that cannabidiol may be an effective strategy for reducing seizures in medically refractory seizures. The flaw with the study is that the doses at the higher end may have been too high for the patients to tolerate, a lower titrated dose may have been equally effective in controlling seizures and minimizing side effects. Nevertheless, the results were promising as it proves to be beneficial in controlling some of the seizures.





  1. Devinsky, et al, “Cannabidiol in patients with treatment-resistant epilepsy: an open-label interventional trial,” Lancet Neurology, 2016, Mar., 15(3):270-280.
  2. McPartland, et al, “Are cannabidiol and 9 delta tetrahydrocannabivarin negative modulators of the endocannabinoid system? A systematic review,” British Journal of Pharmacology, 2015, Feb., 172(3):737-53.
  3. Gaston, et al, “Pharmacology of cannabinoids in the treatment of epilepsy,” Epilepsy Behavior, 2017, May, 70(Pt B):313-318.



Ketogenic diet and its variants, modified Atkins diet and medium-chain triglyceride ketogenic diet and control of seizures

Virginia Thornley, M.D, Neurologist, Epileptologist

March 6, 2018


In the past decade, different modifications of the ketogenic diet have evolved given the high intolerance to the side effects of the classic ketogenic diet and poor adherence to the strict regimen. Other variants have had similar effects in achieving control of seizures. The ketogenic diet remains a viable treatment option in patients medically refractory to conventional agents and should not be discounted as part of the armamentarium of the epileptologist or neurologist who treats patients with seizures.



Studies and classic ketogenic diet

In one small trial of febrile related seizures, 7 children with medically refractory febrile infection-related epilepsy syndrome (FIRES)were followed, 6 had less frequent and less severe seizures. On average, 4 antiepileptic agents were weaned (1). FIRES is a febrile related convulsion syndrome that starts during childhood where febrile seizures are thought to induce a cytokine reaction that occurs post-infectiously(2). In one remarkable study of 77 patients with refractory status epilepticus, only one patient had a shortened acute phase in response to ketogenic diet, 2 to anesthesia and 1 in response to IVIG, all other treatment modalities including conventional IV medications failed to shorten the acute phase (6).


In several case reports of pediatric patients in status epilepticus, the ketogenic diet was used to stop the continuous seizures. In 10 patients in one case series, all 10 pediatric patients were in continuous status epilepticus. 4 patients had focal partial status epilepticus while 6 had generalized status epilepticus. The patients had a mean duration of seizures of 18 days. The mean time for achievement of ketosis was 7 days of which 9/10 patients stopped having continuous seizures during that timeframe(4).

Modified Atkins diet and seizure control

In one study of 14 patients, the modified Atkins diet seemed to be better tolerated than the ketogenic diet. The diet was well-tolerated by 86%. 7 (50%)remained on the diet after 6 months and 36% had a 50% reduction in seizures 21% were seizure free. Strong ketosis appeared to be key in controlling the seizures (5).

Medium chain triglyceride ketogenic diet 

In another variation, the medium-chain triglyceride ketogenic diet, ketones have been challenged as the substrate for control of seizures. It has been shown that medium-chain fatty acids can work through the AMPA receptors where the excitatory neurotransmitter glutamate binds, as the mechanism for controlling seizures and by changing the bioenergetics of the mitochondria (3).





  1. Gofshteyn, et al, “Cannabidiol as a potential treatment for febrile infection-related epilepsy syndrome in acute and chronic phases,” Journal of Child Neurology, 2017, Jan.,32(1):35-40.
  2. Gaspard, et al “New onset refractory epilepticus (NORSE) and febrile infection-related epilepsy syndromes (FIRES): state of the art and perspective,” Epilepsia, 2018, Feb., doi:10:1111/epi. 14022 (Epub ahead of print)
  3. Augustin, et al, “mechanism of action for the medium-chain triglyceride ketogenic diet in neurological and metabolic disorder,” Lancet Neurology, 2018, Jan., 17(1):84-93.
  4. Appavu, et al, “Ketogenic diet treatment for pediatric super-refractory status epilepticus,” Seizure, 2016, Oct., 41:62-65.
  5. Kang, et al, “Use of modified Atkins diet in intractable childhood epilepsy,” Epilepsia, 2007, Jan. 48(1):182-186.
  6. Kramer, et al, “Febrile infection-related epilepsy syndrome(FIRES): pathogenesis, treatment, and outcome: a multicenter study on 77 children,” Epilepsia, 2011, Nov., 52 (11):1956-1967.





Ketogenic diet and its variants modifed Atkins diet, low glycemic index treatment: effectiveness, side effect profile in patients with epilepsy and incidental weight loss

Virginia Thornley, M.D., Neurologist, Epileptologist, February 26, 2018

Doctors first took notice of the ketogenic diet working in patients with epilepsy in the 1920’s. But the exact mechanism remains unclear. One study elucidated that the ketone bodies are one of the reasons why the ketogenic diet works in patients with epilepsy. Ketosis occurs during a natural fasting state. In the ketogenic diet using high fat, the by-products of beta-oxidation of fatty acids which are beta-hydroxyacetate and acetoacetate in the blood do not correlate with patients who are doing better. Medium chain triglyceride fatty acids, which are a part of a variation of the ketogenic diet, are shown to suppress the AMPA receptors which subserve the excitatory neurotransmitter glutamate and may change energy use of the cell through mitochondrial processes (1).


Ketogenic diet and adverse effects

Some patients have difficulty adhering to the diet which makes it difficult to use. Common side effects because of the high-fat content are diarrhea, constipation, nausea, transient increase in lipemic values. Variations of the ketogenic diet are sometimes used to offset these side effects and reduce the non-compliance.

Some ketogenic variants

Ketogenic diet variants include modified Atkins diet, low glycemic index treatment, and medium chain diet. The ketogenic diet consists of 4:1 ratio of fat to carbohydrates shifting metabolism to the use of ketone bodies as a source of energy. A lower ratio is sometimes employed called the modified ketogenic diet with a 3:1 or 2:1 ratio of fat to carbohydrates. In the modified ketogenic diet, the palatability is improved and avoids the gastrointestinal symptoms associated with the ketogenic diet such as nausea. With the modified Atkins diet, carbohydrates are restricted to 10-20 grams a day, or a 1-2:1 ratio of protein to fat plus carbohydrates. In the low glycemic index treatment, carbohydrates are limited to 40-60 grams while 50-60% of the diet is fat and 20-30% is from protein. The medium-chain triglyceride diet employs oils as a supplement such as coconut oil. The palatability of these diets improve patient compliance and lessen the side effects of the ketogenic diet. Some patients also used the diets to incidentally lose weight in addition to treating seizures (2).


Effectiveness of the ketogenic diet and ketogenic diet variants

One study summarizing studies on patients using the classic ketogenic diet found that 50% of patients out of 206 had a >50% reduction of seizures using the classic ketogenic diet. Older patients seemed to benefit less. In the modified Atkins diet, seizures were reduced in younger patients with more frequent seizures. Patients tended to drop out because of the side effects, lack of perceived effectiveness and because of the restrictions in the diet. Patients greater than 12 years old were less adherent to the diet (3).

It is possible that the protective effects of the ketogenic diet are related to the medium chain triglyceride fatty acids and not the ketone bodies.





1. Augustin, et al, “Mechanism of action for medium-chain triglyceride ketogenic diet and metabolic disorders,” Lancet Neurology, 2018, Jan., 84-93.

2. McDonald, et al, “Ketogenic diets for adults with highly refractory epilepsy,” Epilepsy Currents, 2017, Nov.-Dec., 17(6):346-350.

3. Payne, et al, “The ketogenic and related diets in adolescents and adults-a review,” Epilepsia, 2011, Oct., 52(11):1941-1948.

Epilepsy, Uncategorized

Dravet syndrome: clinical course, SCN1A genetic abnormality involved and non-pharmacologic options including ketogenic diet and cannabidiol

By: Virginia Thornley, M.D., Epileptologist, General Neurologist

February 20, 2018

Dravet first described the syndrome that now bears his name in 1978. It is now a model for some of the channelopathies seen manifesting as epilepsy.

Clinical course and electroencephalographic manifestations

Dravet syndrome is also known as the severe myoclonic epilepsy in infancy (SMEI). Patients usually have no delay in development prior to the first seizure. It usually starts between 5-8 months of life another report mentions after 2nd year of life and may follow a febrile seizure. It consists of generalized tonic-clonic seizures and myoclonus. The term severe myocolic epilepsy of infancy (SMEI) is a misnomer as some patients with this gene related disorder may not manifest with myoclonus so Dravet syndrome is preferred. Clinical evolution includes an initial presentation of generalized tonic-clonic seizures evolving into multiple seizure types predominantly myoclonus. Complex partial seizures, focal seizures, and atypical absence seizures may be identified. Myoclonus is seen about 2 years of age and eventually disappears. The generalized type of seizures persists into adulthood. The EEG background becomes progressively slower, with poor organization. There is the presence of excessive frontal theta rhythms and discharges consist of spike, spike and wave and polyspike and wave complexes. There is sensitivity to fevers. It is usually associated with cognitive impairment. Lifespan is unclear as case series are not reported on those after 20 years of age (1).

SCN1A gene

Dravet syndrome is found to be one of the SCN1A-related disorders causing seizures. Genetic testing reveals a heterozygous variant of SCN1A. SCN1A encodes Nav1.1 or the alpha subunit of the voltage-gated sodium channel. Seizures related to this channel are channelopathies. Due to the molecular abnormality at the level of the channel, there is hyperexcitability due to the imbalance of excitation versus inhibition because of neuronal dysfunction at the level of the sodium channel. The SCN1A is encoded on chromosome 2q24 which also includes SCN2A and SCN3A. In epilepsy-associated variants which are all found in the Nav1.1 alpha subunit, they are more frequently found in the C-terminus, and some in the N-terminus. In Dravet syndrome, nearly 50% are truncating variants, while others are splice, missense or deletion types of abnormalities.  The pathophysiology is an area under intense investigation but likely due to loss of the excitability of inhibitory function of the GABAergic pathway causing seizures(4).

Non-pharmacologic ways to deal with conditions of Dravet syndrome

Anti-convulsants to avoid

Prescription agents are not discussed as new agents become available year to year. However, there are medications that should be avoided including carbamazepine, lamotrigine, vigabatrin, and phenytoin. Rufinamide is a similar agent to carbamazepine and could theoretically worsen this condition. Sodium channel blockers like these worsen these types of seizure. In Dravet syndrome,  there is an abnormality of voltage-gated sodium channel Nav1.1, where one would think there would be fewer seizures following the thinking that sodium channel blockers are used anticonvulsants. However, with the sodium channel abnormality in SCN1A seizure disorders, there is more inhibition of the GABAergic pathway which keeps seizures in check thus, there are more excitatory neurotransmitters available causing seizures to occur(4).

Ketogenic diet and mechanisms of action

The ketogenic diet has been found to improve the condition. With ketogenesis, instead of glucose being used as a substrate for seizures, there are increased ketones available from a high fatty acid diet in the body meaning less available glucose that helps keep up the metabolism required with energy expenditure used in seizures. The body uses ketones as the fuel source. Ketogenesis occurs with natural fasting when the body breaks down fat through lipolysis. Then, the fatty acids produced undergo beta-oxidation into ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone) which are used to produce energy ATP (adenosine triphosphate) used by the cells(3). The ketogenic diet mimics this natural process by using a high fat low carbohydrate diet so that instead of glucose the body uses fatty acids which turn into ketones used as a fuel source which is not conducive to seizures.  With ketogenic diet as a therapeutic option, it is key to see a dietician as the diet is strictly high fat. It is based on a tightly regimented all or none principle otherwise it will not work. Most patients eventually find the diet highly unpalatable and may give up. However, if followed faithfully, it may be a viable non-pharmacologic additional option in medically refractory patients with seizures. One study found a 62% reduction rate in Dravet syndrome using the ketogenic diet(2). In the study, the EEG significantly improved and a favorable outcome was seen in those with a shorter duration of the condition and those with generalized tonic-clonic seizures. However, like most studies of rare diseases the number studied was small.


Other mechanisms proposed include changing the pH of the brain making it less favorable for the production of seizures, direct inhibition of ion channels by ketone bodies, and changes in amino acid metabolism to favoring GABAergic synthesis which is inhibitory to seizures.

Cannabidiol in Dravet syndrome

One study examining the effects of cannabidiol (CBD) on Dravet syndrome postulate mechanisms including increasing excitation of the inhibitory effect of the hippocampus where seizures are propagated.  At low doses, it helps with autism and impaired cognition.  It may exert its effect by working against GPR55. The effects of CBD on neurotransmitters were similar to the GPR55 antagonist suggesting CBD works at the level of this lipid-activating G-protein coupled receptor(5).

Consult with your neurologist.






1. Akiyama, et al, “Dravet Syndrome: A Genetic Epileptic Disorder,”Acta Med. Okayama, 2012, 66(5):369-376.

2. Dressler, et al, “Long-term outcome and tolerability of ketogenic diet in childhood epilepsy— the Austrian experience,”Seizure, 2010, Sept., 19(17):404-408.

3. Maranano, et al, “The ketogenic diet: uses in seizures and other neurologic illness,” Current Treatment Options in Neurology, 2008, Nov., 10(6)410-419.

4. Miller, et al, “SCN1A-Related Seizure Disorder,” Gene Reviews, 2007, Nov., Updated 2014, May.

5. Kaplan, et al, “Cannabidiol attenuates seizures and social deficits in a mouse model in Dravet syndrome,” Proceedings of the National Academy of Science, 2017, Oct.


Epilepsy, pain

Cannabidiol: Is there any scientific evidence? Review of some of the novel mechanisms of action in analgesic, anti-epileptic, anti-inflammatory, anti-tumorigenic and anxiolytic effects 

Virginia Thornley, M.D., General Neurologist and Epileptologist


February 16, 2018


Cannabidiol (CBD) is the little known medical component without the euphoria used for medical indications such as analgesic, anti-inflammatory, anti-epileptic and anxiolytic effects. In the pathway for endocannabinoids, cannabinoid exerts its therapeutic effects by binding to the CBD1 receptor found in the brains and the nerves exerting their analgesic effects. CBD does not have the same euphoriant effect as THC its counterpart which is better known to the public with much stigma. CBD will need to be 100 times more potent to have the same euphoria as THC making it relatively safe to give without the intoxicating effects. THC or delta-tetrahydrocannabidiol is the main psychoactive component in the marijuana plant, the one finds in the street drugs which has caused such a stigma shadowing the beneficial effects of the plant. Cannabidiol is also thought to work on the 5HT1 receptor giving its anxiolytic properties. This review seeks to understand some of the laboratory research that study the underlying mechanisms for its beneficial actions.

Cannabidiol works on CBD1 receptor and is thought to have an analgesic and anti-inflammatory role in diseases. In many states, it still outlawed to have in possession but growing clinical evidence shows that it can be used in pain syndromes. In the state of Florida there are 10 conditions recognized that can be treated with CBD. It is most commonly used in pain from stage IV metastatic cancer. Cannabidiol has been found to have anti-inflammatory, anti-tumorigenic, analgesic, anti-epileptic and anxiolytic properties.

Analgesic effects

CB1 receptors are found to be expressed in anterior horn cells. The CB2 receptors possibly reduce pain by acting on the neutrophil accumulation and mast cell degranulation which can reduce pain both of these processes increase inflammatory algesia(1).Analgesia has been demonstrated with cannabinoids in visceral inflammation and pain due to peripheral neuropathies, important areas of therapeutic considerations.

Anti-seizure effects

Some of the vast scientific research for cannabinoid is found in the animal models for epilepsy. Cannabinoids exert effects on CB1 and CB2 receptors in the hippocampus where it has a weak affinity(5). CBD1 receptors affect transmission in the synapses through the voltage-gated calcium and potassium channels. There are studies on the effects of CBD in refractory types of epilepsy such as Dravet’s syndrome one of the SCN1a genetic disorders affecting the sodium channel manifesting as severe myoclonic epilepsy. Mechanisms of CBD include increasing excitation of the inhibitory effect of the hippocampus where seizures are propagated.  At low doses, it helps with autism and impaired cognition.  It may exert its effect by working against GPR55(7), TRPV1 in addition to voltage-gated voltage-gated potassium and sodium channels. Another study supports the role that cannabinoids may play in shifting the inhibition of glutamatergic effects and GABAergic effects in the hippocampus mediated by CB1 receptors. In the rat model, it was suggested that seizures can upset the balance of these glutamate and GABA systems (4). 15 minutes after an induced seizure, there is increased 2-arachidonylycerol which is a CB1 agonist suggesting cannabinoids act as a negative feedback loop for seizures(4). In addition, it was found there are more CB1 receptors in the hippocampi with induced seizures compared to control suggesting plasticity of the brain with a compensatory increase in CB1 receptors in response to increased seizures(4). CB2 receptors are related to the immune system and are limited in the CNS. Cannabinoids affect calcium homeostasis and may provide its neuroprotective effects. Growing evidence shows case series, case reports and anecdotal reports on patients having fewer seizures on cannabidiol. Large case-controlled clinical randomized trials are needed.

Anti-tumor effects

There appears to be increased cancel cell death, reduced viability and reduced numbers of metastatic cells. In one study, it is found to reduce epidermal growth factor-induced multiplication and chemotaxis of cells in breast cancer. In mouse models, it inhibits macrophage recruitment in tumor-related cells.n It can potentially inhibit metastasis and proliferation and may provide a novel therapeutic option in breast cancer(2).

Anxiolytic effects

It works on the 5HT1 receptor by altering effects on this receptor the exact mechanism is unknown accounting for anxiolytic properties(6).


Anti-psychotic effects

CBD may alter the effects of THC and reduce its psychoactive properties (6).


Alternative treatment in opioid use

CBD might also work in place of opioids with the growing epidemic of chronic pain and overuse of opioids, CBD may be an alternative analgesic for chronic pain without the effect of tolerance or sedating properties. CBD was found to reduce the reward effects of morphine and does not have the same properties of tolerance. CBD does not have the same euphoria and THC and works on pain(6).

In summary, it is an exciting time for research in the use of cannabinoids. There are innumerable basic science research studies demonstrating the therapeutic effects at the cellular level. Large randomized clinical trials are still needed to gain information in using cannabinoids in humans.





1. Rice, AS, et al, “Endocannabinoids and pain: peripheral and spinal analgesia in inflammation and neuropathy, ” Prostaglandins, Leukotrienes and Essential Fatty Acids, 2002, Feb., 66(2-3)246-256.

2. Elbaz, E. et al, ” Modulation of tumor microenvironment and inhibition of EGF/EGFR pathway: novel mechanisms of Cannabidiol on breast cancer,”Molecular Oncology, 2015, Apr., 9(4):906-919.

3. Welty, W.E., et al, “Cannabinoids: the promises and pitfalls,” Epilepsy Currents, 2014, Sep.-Oct., 14(5):250-252.

4. Wallace, MJ, et al, ” The endogenous Cannabinoid system regulates seizure frequency and duration in a model of temporal lobe epilepsy, ” The Journal of Pharmacology and Experimental Therapeutics, 2003, Oct., 307(1):129-137.

5. Gaston, T. et. al, “Pharmacology of cannabinoids in the treatment of epilepsy, ” Epilepsy Behavior, 2017, May, 70:313-318.

6. Volkow, Nora, “The biology and potential therapeutic effects of cannabidiol,” National Institute on Drug Abuse Senate Caucus on International Narcotics Control, 2015, June.

7. Kaplan, et.al, “Cannabidiol attenuates seizures and social deficits in a mouse model in Dravet syndrome, “Proceedings of the National Academy of Science, 2017, Oct.

Epilepsy, migraine

Sleep Hygiene especially for Migraineurs and those with Epilepsy

By Virginia Thornley, M.D., Neurologist, Epileptologist
February 15, 2018

Many neurological diseases are affected by lack of sleep most significantly migraine and epilepsy. A person performs suboptimally with lack of sleep with inattention and lack of coordination. In someone with a neurological condition, the symptoms become even more manifest. Weakness becomes more prominent, double vision may be more pronounced and difficulty speaking will become more prominent. Sleep plays a vital role in the restorative function of the body.

Stages of sleep, why adequate and continuous sleep is refreshing
Sleep is divided into 2 categories, Non-REM (rapid eye movement) sleep and REM sleep. During non-REM sleep, there are 4 stages. Stage 1 and 2 constitute drowsiness which transitions into light sleep. The electroencephalogram is a study that reflects brain activity. Stages 1 and 2 demonstrates sleep complexes including vertex waves then K complexes. Sleep spindles occur during stage 2 sleep. During stages 3 and 4 also known as slow-wave sleep, delta waves which are the slowest waves between 1-3 Hertz start to occur. Stage 4 shows delta waves of greater than 50% of the recording. People enter these stages of sleep and then subsequent REM sleep. REM sleep is where dreaming occurs.

One can go through a few cycles of these so that you wake up refreshed. Continue reading


By Virginia Thornley, M.D., Neurologist, Epileptologist
February 16, 2018

Epilepsy is a condition involving 2 or more seizures. A seizure occurs when the electrical impulses in the brain do not cease and as a result, become recurrent resulting in excess cerebral activity. Typically, it occurs in the grey matter of the cortex, although seizures can be seen in white matter diseases such as in multiple sclerosis. Manifestations depend on the area involved. Etiologies are vast and are due to underlying structural abnormalities in the brain which may arise due to autoimmune processes, neoplastic causes (cancer), infectious diseases, traumatic etiologies or drug-induced causes. At times, there is no structural damage and may be genetic in predisposition. The seizures are similar in nature because the same underlying part of the brain is activated causing the same type of seizure. Different clinical manifestations signify a different or new area involved. If a seizure spreads to the entire brain it manifests as convulsions with clinical symptoms of loss of consciousness and whole body rhythmic jerking.

What to avoid if you have seizures

Sleep deprivation
Sleep deprivation causes seizures to occur. When the brain is well rested it performs at maximal capacity. When it performs at suboptimal conditions such as sleep deprivation or fatigue, neurological conditions become more manifest.

Missing meals
Missing meals can give rise to seizures. When you miss a meal your blood glucose or sugar is lower. This low level of sugar also known as hypoglycemia can cause seizures to occur.



Certain medications can reduce the threshold of seizures including ciprofloxacine, certain cephalosporins and tramadol. Some psychotropic agents such as clozapine and chlorpromazine can lower the seizure threshold. It is best to avoid these agents and ensure your physicians know all your conditions. Amphetamines can also cause seizures and lower the seizure threshold.

Drugs of abuse
Some drugs are notorious for causing seizures such as cocaine. Cocaine can cause the blood vessels to constrict leading to strokes which can result in brain damage and seizures can result. Alcohol, if consumed by those with a genetic predisposition, can give rise to seizures. Excessive alcohol abuse can give rise to alcohol-induced seizures.

Other lifestyle changes 

Because loss of consciousness may be involved, potential harm can occur. Avoiding heights such as ladders, cliffs, the edges of train platforms or subway platforms can help avert harm. Using the back burner while cooking help prevents burns. Avoiding driving for at least 1 year of seizure freedom can prevent accidents, some states require only 6 months. Avoiding the operation of heavy equipment such as forklifts, cranes can prevent accidents. Avoidance of swimming alone may prevent drowning, same is true with avoidance of taking baths alone.


It is an excellent idea to get a medics alert bracelet especially for young patients who may have a seizure late at night in public. After a seizure, patients may appear incoherent, disoriented and confused. It is also good to keep a list of medications.
Keeping everything clear around the patient can prevent injury.

An excellent resource for information and support is the Epilepsy Foundation. They provide a wealth of non-medical services including support and assistance in job-related issues. Some branches even have summer camps for children.




Epilepsy: Living with Epilepsy

Avoiding heights such as ladders, cliffs, the edges of train platforms or subway platforms can help avert harm. Using the back burner while cooking help prevents burns. Avoiding driving for at least 1 year of seizure freedom can prevent accidents, some states require only 6 months.