How to prevent epilepsy?

Preventing Epilepsy Seizures

Epileptic seizures are often associated with particular triggers or changes in your daily habits or routine. Here are some common behaviors and factors that may trigger an epileptic seizure:

  • Stress, anxiety, or other emotional issues
  • Alcohol or drug abuse or the process of quitting alcohol or drugs
  • Change in sleep schedules, feeling very tired, or significant sleep deprivation
  • A change in medications, or skipping or missing a dose of anti-seizure medication
  • Something that overstimulates the senses, like lights that flash brightly, watching television, playing video or computer games, or working on a computer
  • Hormonal changes in women, often from pregnancy or menstruation
  • Mental strain, such as from solving complex problems

You can’t always predict what will trigger an epileptic seizure; sometimes they’ll occur for no apparent reason. But many people are able to see a correlation between certain behaviors and their seizures. By taking steps to minimize these factors, you may be able to prevent seizures.

Seizure Prevention Tips

Here are some tips that may help reduce your risk of having an epilepsy seizure:

  • Get plenty of sleep each night — set a regular sleep schedule, and stick to it.
  • Learn stress management and relaxation techniques.
  • Avoid drugs and alcohol.
  • Take all of your medications as prescribed by your doctor.
  • Avoid bright, flashing lights and other visual stimuli.
  • Skip TV and computer time whenever possible.
  • Avoid playing video games.
  • Eat a healthy diet.

Until more is known about the causes of epilepsy and how it can be prevented, your best bet to prevent seizures associated with epilepsy is to avoid the things that can trigger your seizures. This can make a measurable difference in the number of seizures you have.

How Can I Prevent Epilepsy?

In someone with epilepsy, certain triggers can lead to a seizure. Identify and watch for particular behaviors, environments, or physical and emotional signs that precede attacks. It’s not uncommon, for example, to feel annoyed or elated several hours prior to a grand mal seizure, and immediately before the attack.

In addition, the person may become aware of a warning “aura” — perhaps a taste or smell: This warning may allow you to lie down in time to avoid falling. In cases where the aura is a smell, some people are able to fight off seizures by sniffing a strong odor, such as garlic or roses. When the preliminary signs include depression, irritability, or headache, an extra dose of medication (with a doctor’s approval) may help prevent an attack. In the case of a Jacksonian seizure, firmly squeezing the muscles around those that are twitching can sometimes halt the attack.

Take precautions if your seizures are not fully controlled. Avoid or limit alcohol, comply with your state’s requirements for a seizure-free period prior to driving a vehicle, and educate family members on steps to minimize injury if you have a seizure. Tell them to protect you against falling, and to roll you onto your side if you lose consciousness.


Epilepsy treatment

Epilepsy usually is treated with medicine. If medicine doesn’t help your seizures, your doctor may recommend surgery or other therapies. If your doctor knows what is causing your epilepsy, treating the cause may make the seizures stop.

What do I need to know about taking medicine for epilepsy?

Medicines that help prevent seizures are called anticonvulsants or antiepileptics. Your doctor will recommend a medicine based on the type of seizures you have, how often you have seizures, your age, and your general health. After you begin taking the medicine, your doctor will monitor you closely to determine whether the drug is working. He or she will also be watching for side effects, and to make sure your dose is correct.

Side effects may include fatigue, dizziness, skin rash, or problems with your memory, coordination, or speech. Call your doctor right away if you experience depression, suicidal thoughts, or severe rash while taking your medicine.

To help your medicine work well, follow your doctor’s instructions for taking it. Do not stop taking your medicine without talking to your doctor. Ask your doctor what to do if you miss a dose. Never take extra medicine, even if you think you’re about to have a seizure. Talk to your doctor before you start taking any new medicines, including vitamins or supplements.

You should avoid drinking alcohol if you have epilepsy. Alcohol can make it easier to have a seizure and can also affect the way your epilepsy medicine works in your body. Some medicines can also make it easier to have a seizure, so check with your doctor before starting to take any new medicines.

It may be possible for some people who have epilepsy to eventually stop taking medicine. However, this decision must be made by your doctor. Before you and your doctor can decide to stop the medicine, several questions should be considered. These include how quickly your seizures were controlled, how long you have been free of seizures, and if you have other illnesses that may affect your problem.

What about surgery and other therapies?

Surgery is most commonly done if it’s known that your seizures begin in a well-defined area of your brain that doesn’t interfere with important functions like speech, language, or hearing. In other cases of medicine-resistant seizures, your doctor may recommend a type of therapy called vagus nerve stimulation. This requires a small device be implanted under the skin on your chest. The device delivers electrical pulses to the vagus nerve in the neck. A kind of treatment for children with certain types of epilepsy that are difficult to control involves a strict diet that is high in fat and low in carbohydrates. This diet is known as a ketogenic diet. This diet should be prescribed and monitored by a physician. With all treatments, work with your doctor to determine the best treatment for you.

What should I do when someone has a seizure?

If you have epilepsy, you may want to share the following information with your family, friends, and coworkers. If someone near you has a seizure, use the following general guidelines:

  • Stay calm.
  • Don’t move the person to another place.
  • Don’t try to keep the person from moving or shaking.
  • Don’t try to wake the person by shouting at or shaking them.
  • Remove items that could cause injury if the person falls or bumps into them.
  • Gently turn the person on his or her side so any fluid in the mouth can safely come out.
  • Never try to force the person’s mouth open or put anything in it.
  • Place something soft (such as a pillow) under his or her head.
  • Most seizures aren’t life-threatening. You don’t need to call a doctor or an ambulance unless the person isn’t known to have epilepsy or unless the seizure lasts longer than 5 minutes.
  • When the seizure is over, watch the person for signs of confusion.
  • Allow the person to rest or sleep if he or she wishes.

Can natural treatments help with epilepsy?

People with epilepsy and their doctors are expressing growing interest in alternative therapies.

Although antiepileptic drugs (AEDs) help most people control their symptoms, these do not work for everyone. Furthermore, some people are concerned about the long-term safety of these drugs.

Complementary health practices for epilepsy, such as the eight natural remedies discussed here, are designed for use in combination with AEDs.

After talking to a doctor, and before beginning natural treatments, people with epilepsy should ensure they are working with a well-qualified and informed therapist.

Common complementary treatments for epilepsy include the following:

Medical marijuana

Cannabis sativa, or marijuana, as it is commonly known, has been used to treat convulsions for centuries. Today, it is attracting increasing attention from people with epilepsy, clinicians, and researchers.

Interest in the use of medical marijuana is particularly strong for the roughly 1 million U.S. residents whose seizures are not controlled by AEDs. Some families with young children, suffering from severe seizures, have moved to one of the 22 states where medical marijuana use is legal.

Charlotte’s Web is a strain of cannabis bred to contain high levels of CBD, a part of the plant showing promise against seizures. It is named after a child whose convulsions dropped from more than 300 a week to 2-3 a month with this treatment.

However, since broad-based, well-designed scientific studies have yet to prove the effectiveness of marijuana in treating epilepsy, doctors do not generally recommend its use.


Share on PinterestThe ketogenic diet is a low-carbohydrate, high-fat diet that may help to reduce seizures.

Diet is one of the earliest forms of treatment for epilepsy and is used with contemporary variations to make it easier for children and adults to adopt.

The ketogenic diet is a high-fat, low-carbohydrate diet that has had some success in reducing seizures in children who cannot tolerate or benefit from AEDs. It requires extensive commitment and monitoring.

The Atkins diet is a high-protein, low-carbohydrate diet that is less restrictive and has shown positive effects.

Low glycemic index treatment (LGIT) is similar but allows for a targeted level of carbohydrate consumption.

Herbal treatments

Herbs are used for many illnesses by 80 percent of the world’s population. Remedies drawing on Chinese traditions have shown promise in treating epilepsy.

Some herbs, such as chamomile, passionflower, and valerian, may make AEDs more effective and calming.

However, ginkgo, ginseng, and stimulating herbs containing caffeine and ephedrine can make seizures worse.

St. John’s wort can interfere with medications and make seizures more likely, similarly to evening primrose and borage.

Caution is advised when working with all these herbs.

It is important to remember that herbs are not monitored by the U.S. Food and Drug Administration (FDA). If any herbs are used, they should be researched and bought from reputable sources.


Low levels of the B6 vitamin have been known to trigger seizures.

Magnesium, vitamin E, and other vitamins and nutritional supplements, have been identified as either promising or problematic for treating epilepsy.

People taking AEDs are often advised to take vitamin D supplements to keep their systems in balance.

Along with vitamin B6, magnesium, and vitamin E, which have been found to be helpful in treating epilepsy, doctors have found treatment with manganese and taurine reduced seizures, as well.

Thiamine may help improve the ability to think in people with epilepsy.


When AEDs do not work, some people have successfully used biofeedback to reduce seizures.

With the use of extensive training and a machine that detects electrical activity in the brain, the technique teaches individuals to recognize the warning signs of seizures, and train their brains to prevent a full-blown attack.


Stress and anxiety are both linked to seizures.

There are many different practices that people with epilepsy can follow on their own to help them feel calmer, relax their muscles, get better sleep, and enjoy a better state of mind.

All these actions taken together can help reduce seizures and make it easier for people to manage their epilepsy.

People should be cautious if trying meditation, as this can change the electrical signals in the brain.

Some essential oils used in aromatherapy, such as lavender, chamomile, jasmine, and ylang-ylang, have been found to be effective in preventing seizures when used with relaxation techniques.

However, the Epilepsy Society report that others may provoke seizures. These include spike lavender, eucalyptus, camphor, sage, rosemary, hyssop, and fennel.

Acupuncture and chiropractic

Share on PinterestAcupuncture may help to reduce the stress of living with epilepsy.

While acupuncture does not seem to be helpful in preventing seizures, people with epilepsy find it can reduce the stress of living with the condition.
There is little evidence on chiropractic care, but it also may be among the natural treatments people with epilepsy find useful.

Education and avoiding triggers

Education and avoidance can have a big impact on quality of life for people with this condition.

Many of those with epilepsy find that their seizures develop in response to specific triggers. This is the case for people with photosensitive epilepsy.

Learning how to avoid situations and stimuli that could spark a seizure can be very helpful. Some children may learn to avoid using video games in dark rooms, for example, or to cover one eye when exposed to flashing lights.

How Can You Prevent a Seizure From Happening?

Our first post gave information on the definition of epilepsy and “What To Do If Someone Has a Seizure,” so next you may be wondering can it be prevented? At present, the only way of preventing epilepsy is by reducing risks from things that damage the brain. Research may one day provide ways to identify people at risk of seizures and to prevent epilepsy before it begins.

Since the cause of epilepsy is still unknown, it can’t be fully prevented, but the seizures associated with epilepsy can be, and here are a few of those methods used by parents and individuals with epilepsy for seizure prevention:

1. Seizure Medications: Children and/or individuals with epilepsy can gain control of their seizures with regular use of seizure-preventing medicines. These medicines have to be taken from one to four times a day– depending on what is prescribed in their treatment regimen by the neurologist/epileptologist. Successful treatment depends on keeping a steady level of medication in the blood at all times, so it is important that doses not be missed or given late. One thing to keep in mind is that medications work differently for each individual and/or child. What works for some may not for others, and there is no quick fix when it comes to epilepsy.

2. Ketogenic Diet: The ketogenic diet is one of the oldest treatments for epilepsy. It is intended to maintain the starvation or fasting metabolism over a long period of time. When the body is in a fasting state, it creates ketones, a by-product of fat-burning metabolism. It has long been recognized that seizures often lessen or disappear during periods of fasting in some individuals with epilepsy.

The diet is very high in fat and low in carbohydrates. When fat is the primary source of calories, ketones are formed. The diet must be followed very strictly and requires a significant commitment to work effectively. Children on the diet often will not gain weight or grow much during the time the diet is in use. After that, however, growth is expected and should be carefully monitored.

The diet is typically started with a period of fasting lasting until the body produces a moderate to large amount of ketones. This initiation period usually takes place in the hospital, so that the individual can be monitored for potential side effects such as vomiting, low blood sugar, dehydration and seizures. Medications may also be adjusted during this period to prevent sedation (the tranquilizing effect of medications), another common side effect.

A two-month trial period is suggested for deciding whether the diet is effective. If effective, it is typically continued for two years. During this time, individuals are often able to lessen the amount of medication they take for seizures. Many children seem happier and more alert on the diet, even before medication is significantly lessened. People on a ketogenic diet should be monitored by a dietician, nurse and doctor particularly a neurologist familiar with its use. Specialized epilepsy clinics are available to monitor a person on this diet.

3. VNS Therapy (Vagus Nerve Stimulator): VNS therapy is not brain surgery. VNS therapy involves a minimally invasive procedure, which is typically performed under general anesthesia by a surgeon. The procedure takes approximately one hour, and patients usually go home the same day. Typically, two small incisions are made— one in a natural crease on the left side of the neck and one in the left chest area, below the collarbone. The generator is typically placed under the skin in the left chest area. A thin, flexible wire connects the generator to the left vagus nerve in the neck. The small scars from the two incisions typically fade over time and become minimally noticeable for many people. Another procedure is required to replace the generator once the battery is depleted. This procedure requires only one incision and usually takes less than an hour. The VNS therapy procedure is completely reversible.

For those who benefit from VNS therapy, it has been clinically proven to reduce the number and intensity of seizures and, in some cases, to completely eliminate seizures. Studies show that, unlike a medication, the effects of VNS therapy may take between a few months to one or two years to reach optimum levels. The positive effects of VNS therapy are long-lasting, typically do not decline, and may, in fact, improve over time. In addition, many patients using VNS therapy have also reported improvements in mood, increased alertness and enhanced memory. Furthermore, physicians have confirmed that some patients have been able to reduce the quantity and/or doses of medication over time. Many patients using VNS therapy no longer have to make as many visits to the hospital. VNS therapy is an added treatment to your current medications. It is not a replacement for them.

For more information please, go to the Epileps Warriors Foundation website.

About Susan Noble and the Epilepsy Warriors

As President and Founder of the Epilepsy Warriors, Susan Noble is striving to reach as many people within the local communities to help educate and bring an end to the stigma of epilepsy. It takes team work. It involves supporting each other in all efforts. It means showing the world that epilepsy is worth researching, fighting for and funding. We are all fighting for a CURE for our children and those “living with epilepsy” every day. We are a new foundation– one with a passionate vision. This vision will light our path and guide us towards our goals of “enlightening, empowering and curing.”
Susan and her family reside in Fort Myers, Florida otherwise known as her little slice of paradise.

An epileptic seizure is a frightening thing to experience, and almost as frightening to watch. The person loses consciousness and falls to the ground. His or her muscles contract in spasms, causing uncontrollable jerks and twitches. Spasms of the jaw muscles can cause the person to bite his or her tongue. Breathing becomes difficult, and may even stop briefly. Seizures cause some people to lose control of their bladder or bowels.

Fortunately, most seizures stop on their own after a couple minutes. Any that last longer than five to 10 minutes (doctors call such long-lasting seizures status epilepticus) are a medical emergency and must be halted with medication administered intravenously by a doctor or emergency medical technician. More than 50,000 people in the United States die from prolonged seizures every year, either from brain damage due to the seizure itself or from accidents related to passing out mid-attack.

A study published last week in the New England Journal of Medicine indicates that a hand-held auto-injector—much like the epi pens used by people with life-threatening allergies—could be used to treat seizures that don’t stop on their own. This could pave the way for home treatment of epileptic seizures.

Muscle trumps vein

For the trial, more than 4,000 emergency medical technicians were trained to administer seizure-stopping drugs called benzodiazepines two ways: through an intravenous line inserted into a vein in the arm (the current standard treatment), and with a device that automatically injects the drug into the thigh. Intravenous administration works faster, but it can be hard to put an intravenous line into the arm of someone having a seizure. Injection into the thigh takes effect a bit more slowly, but is far easier to do.

Over an 18-month period, emergency medical crews responded to 893 long-lasting seizures. Half of the people in status epilepticus received a benzodiazepine intravenously, the other half by thigh injection. The muscle injection worked faster and better. It stopped the seizure in 73% of the people before they arrived at the hospital. The intravenous route stopped the seizure in 63%.

Minutes matter

Seizures that end quickly don’t damage the brain. Those that last longer than five minutes can cause permanent brain damage and disability. The longer a seizure goes on past 10 minutes, the harder it is to stop it with medication. And up to one in five people die from a long-lasting seizure. So the sooner an anti-seizure medication can reach the brain, the better.

If you ever witness a seizure, stay calm and do your best to keep everyone else calm. Here are some steps you can take:

Call 911, or have someone else do it.

Time the seizure. This information will be helpful when the emergency medical crew arrives. Try to remember as many details as you can to tell the paramedics and doctor later.

Provide support. Don’t try to hold the person down or force anything into his or her mouth, even if the tongue is bleeding. To prevent head injury, gently position a soft, flat object like a jacket under the head. Remove any hard or sharp objects that are near the person.

When the jerking stops, gently roll the person onto his or her side. When the person wakes up, be reassuring and provide transportation or other help that may be needed.

Looking ahead

This one study isn’t the green light for doctors to give auto-injectors filled with anti-seizure medication to all of their patients who have seizures. With further testing for safety, though, that is likely to happen. This could spare these people and their families the agonizing wait for an ambulance to arrive in order to halt the seizure. Proper education on the use of these injectors will also be important.

In addition to auto-injectors, researchers are also testing a nasal spray containing a benzodiazepine. This could deliver the medication to the brain even faster than an auto-injector.


  • Ackermann RF, Finch DM, Babb TL, Engel J., Jr Increased glucose metabolism during long-duration recurrent inhibition of hippocampal pyramidal cells. J Neurosci. 1984;4:251–264.
  • Albala BJ, Moshe SL, Cubells JF, Sharpless NS, Makman MH. Unilateral peri-substantia nigra catecholaminergic lesion and amygdale kindling. Brain Res. 1986;370:388–392.
  • Alger BE, Nicoll RA. Epileptiform burst after hyperolarization: calcium-dependent potassium potential in hippocampal CA1 pyramidal cells. Science. 1980;210:1122–1124.
  • Auer RN. Progress review: hypoglycemic brain damage. Stroke. 1986;17:699–708.
  • Ayala GF. The paroxysmal depolarizing shift. Prog Clin Biol Res. 1983;124:15–21.
  • Ayala GF, Dichter M, Gumnit RJ, Matsumoto H, Spencer WA. Genesis of epileptic interictal spikes. New knowledge of cortical feedback systems suggests a neurophysiological explanation of brief paroxysms. Brain Res. 1973;52:1–17.
  • Baraban SC, Hollopeter G, Erickson JC, Schwartzkroin PA, Palmiter RD. Knock-out mice reveal a critical antiepileptic role for neuropeptide Y. J Neurosci. 1997;17:8927–8936.
  • Beierlein M, Gibson JR, Connors BW. A network of electrically coupled interneurons drives synchronized inhibition in neocortex. Nat Neurosci. 2000;3:904–910.
  • Bellmann R, Widmann R, Olenik C, Meyer DK, Maas D, Marksteiner J, Sperk G. Enhanced rate of expression and biosynthesis of neuropeptide Y after kainic acid-induced seizures. J Neurochem. 1991;56:525–530.
  • Benarroch EE. Neuron-astrocyte interactions: partnership for normal function and disease in the central nervous system. Mayo Clin Proc. 2005;80:1326–1338.
  • Bikson M, Hahn PJ, Fox JE, Jeffreys JG. Depolarization block of neurons during maintenance of electrographic seizures. J Neurophysiol. 2003;90:2402–2408.
  • Boison D. Adenosine and epilepsy: from therapeutic rationale to new therapeutic strategies. Neuroscientist. 2005;11:25–36.
  • Bragin A, Penttonen M, Buzsaki G. Termination of epileptic after-discharge in the hippocampus. J Neurosci. 1997;17:2567–2579.
  • Brooks-Kayal AR. Rearranging receptors. Epilepsia. 2005;46 (Suppl. 7):29–38.
  • Bullock TH, Bennett MV, Johnston D, Josephson R, Marder E, Fields RD. Neuroscience. The neuron doctrine, redux. Science. 2005;310:791–793.
  • Carpenter LL, Moreno FA, Kling MA, Anderson GM, Regenold WT, Labiner DM, Price LH. Effect of vagus nerve stimulation on cerebrospinal fluid monoamine metabolites, norepinephrine, and gamma-aminobutyric acid concentrations in depressed patients. Biol Psychiatry. 2004;56:418–426.
  • Chabardes S, Kahane P, Minotti L, Koudsie A, Hirsch E, Benabid AL. Deep brain stimulation in epilepsy with particular reference to the subthalamic nucleus. Epileptic Disord. 2002;4 (Suppl. 3):S83–S93.
  • Chen L, Chan YS, Yung WH. GABA-B receptor activation in the rat globus pallidus potently suppresses pentylenetetrazol-induced tonic seizures. J Biomed Sci. 2004;11:457–464.
  • Chen JW, Naylor DE, Wasterlain CG. Advances in the pathophysiology of status epilepticus. Acta Neurol Scand Suppl. 2007;186:7–15.
  • Chesler M, Kraig RP. Intracellular pH of astrocytes increases rapidly with cortical stimulation. Am J Physiol. 1987;253:R666–R670.
  • Chesler M, Kaila K. Modulation of pH by neuronal activity. Trends Neurosci. 1992;15:396–402.
  • Chudomel O, Galanopoulou A, Moshè S. Tonic and phasic GABA currents in GABAergic neurons of the substantia nigra reticulata are dependent on age regardless of sex. American Epilepsy Society Annual Meeting, San Diego. 2006
  • Cohen JE, Fields RD. Extracellular calcium depletion in synaptic transmission. Neuroscientist. 2004;10:12–17.
  • Colmers WF, El Bahh B. Neuropeptide Y and epilepsy. Epilepsy Curr. 2003;3:53–58.
  • Connors BW, Cruikshank SJ. Bypassing interneurons: inhibition in neocortex. Nat Neurosci. 2007;10:808–810.
  • Coulter DA, DeLorenzo RJ. Basic mechanisms of status epilepticus. Adv Neurol. 1999;79:725–733.
  • Crawford TO, Mitchell WG, Snodgrass SR. Lorazepam in childhood status epilepticus and serial seizures: effectiveness and tachyphylaxis. Neurology. 1987;37:190–195.
  • Cruikshank SJ, Lewis TJ, Connors BW. Synaptic basis for intense thalamocortical activation of feedforward inhibitory cells in neocortex. Nat Neurosci. 2007;10:462–468.
  • de Curtis M, Manfridi A, Biella G. Activity-dependent pH shifts and periodic recurrence of spontaneous interictal spikes in a model of focal epileptogenesis. J Neurosci. 1998;18:7543–7551.
  • DeFelipe J, Farinas I. The pyramidal neuron of the cerebral cortex: morphological and chemical characteristics of the synaptic inputs. Prog Neurobiol. 1992;39:563–607.
  • DeLorenzo RJ, Towne AR, Pellock JM, Ko D. Status epilepticus in children, adults, and the elderly. Epilepsia. 1992;33 (Suppl. 4):S15–S25.
  • DeVries SH, Schwartz EA. Modulation of an electrical synapse between solitary pairs of catfish horizontal cells by dopamine and second messengers. J Physiol. 1989;414:351–375.
  • Dichter M, Spencer WA. Penicillin-induced interictal discharges from the cat hippocampus. II. Mechanisms underlying origin and restriction. J Neurophysiol. 1969;32:663–687.
  • Dorn T, Witte OW. Refractory periods following interictal spikes in acute experimentally induced epileptic foci. Electroencephalogr Clin Neurophysiol. 1995;94:80–85.
  • Dragunow M, Goddard GV, Laverty R. Is adenosine an endogenous anticonvulsant? Epilepsia. 1985;26:480–487.
  • Dube C, Boyet S, Marescaux C, Nehlig A. Progressive metabolic changes underlying the chronic reorganization of brain circuits during the silent phase of the lithium-pilocarpine model of epilepsy in the immature and adult Rat. Exp Neurol. 2000;162:146–157.
  • Dunwiddie TV, Masino SA. The role and regulation of adenosine in the central nervous system. Annu Rev Neurosci. 2001;24:31–55.
  • During MJ, Spencer DD. Adenosine: a potential mediator of seizure arrest and postictal refractoriness. Ann Neurol. 1992;32:618–624.
  • Dzhala VI, Talos DM, Sdrulla DA, Brumback AC, Mathews GC, Benke TA, Delpire E, Jensen FE, Staley KJ. NKCC1 transporter facilitates seizures in the developing brain. Nat Med. 2005;11:1205–1213.
  • Dzhala VI, Brumback AC, Staley KJ. Bumetanide enhances Phenobarbital efficacy in a neonatal seizure model. Ann Neurol. 2008;63:222–235.
  • Erickson JC, Clegg KE, Palmiter RD. Sensitivity to leptin and susceptibility to seizures of mice lacking neuropeptide Y. Nature. 1996;381:415–421.
  • Fedele DE, Gouder N, Guttinger M, Gabernet L, Scheurer L, Rulicke T, Crestani F, Boison D. Astrogliosis in epilepsy leads to overexpression of adenosine kinase, resulting in seizure aggravation. Brain. 2005;128:2383–2395.
  • Gajda Z, Szupera Z, Blazso G, Szente M. Quinine, a blocker of neuronal cx36 channels, suppresses seizure activity in rat neocortex in vivo. Epilepsia. 2005;46:1581–1591.
  • Galanopoulou AS, Moshe SL. Role of sex hormones in the sexually dimorphic expression of KCC2 in rat substantia nigra. Exp Neurol. 2003;184:1003–1009.
  • Galanopoulou AS, Kyrozis A, Claudio OI, Stanton PK, Moshe SL. Sex-specific KCC2 expression and GABA(A) receptor function in rat substantia nigra. Exp Neurol. 2003;183:628–637.
  • Galanopoulou AS, Chudomel O, Heida J, Moshe SL. Neonatal seizures cause long term changes in GABAA receptors in rat substantia nigra. American Epilepsy Society Annual Meeting; American Epilepsy Society; San Diego. 2006.
  • Galanopoulou AS. Developmental patterns in the regulation of chloride homeostasis and GABA(A) receptor signaling by seizures. Epilepsia. 2007;48 (Suppl. 5):14–18.
  • Galarreta M, Hestrin S. Electrical synapses between GABA-releasing interneurons. Nat Rev Neurosci. 2001;2:425–433.
  • Glass M, Faull RL, Bullock JY, Jansen K, Mee EW, Walker EB, Synek BJ, Dragunow M. Loss of A1 adenosine receptors in human temporal lobe epilepsy. Brain Res. 1996;710:56–68.
  • Goodkin HP, Sun C, Yeh JL, Mangan PS, Kapur J. GABA(A) receptor internalization during seizures. Epilepsia. 2007;48 (Suppl. 5):109–113.
  • Gouder N, Scheurer L, Fritschy JM, Boison D. Overexpression of adenosine kinase in epileptic hippocampus contributes to epilepto-genesis. J Neurosci. 2004;24:692–701.
  • Grenier F, Timofeev I, Steriade M. Neocortical very fast oscillations (ripples, 80–200 Hz) during seizures: intracellular correlates. J Neurophysiol. 2003;89:841–852.
  • Groves DA, Brown VJ. Vagal nerve stimulation: a review of its applications and potential mechanisms that mediate its clinical effects. Neurosci Biobehav Rev. 2005;29:493–500.
  • Hamani C, Saint-Cyr JA, Fraser J, Kaplitt M, Lozano AM. The subthalamic nucleus in the context of movement disorders. Brain. 2004;127:4–20.
  • Hamzei-Sichani F, Kamasawa N, Janssen WG, Yasumura T, Davidson KG, Hof PR, Wearne SL, Stewart MG, Young SR, Whittington MA, Rash JE, Traub RD. Gap junctions on hippocampal mossy fiber axons demonstrated by thin-section electron microscopy and freeze fracture replica immunogold labeling. Proc Natl Acad Sci USA. 2007;104:12548–12553.
  • Hasenstaub A, Shu Y, Haider B, Kraushaar U, Duque A, McCormick DA. Inhibitory postsynaptic potentials carry synchronized frequency information in active cortical networks. Neuron. 2005;47:423–435.
  • Haut SR, Veliskova J, Moshe SL. Susceptibility of immature and adult brains to seizure effects. Lancet Neurol. 2004;3:608–617.
  • Heida JG, Veliskova J, Velisek L, Chudomel O, Moshe SL, Galanopoulou AS. Early life status epilepticus alters the seizure controlling function of the substantia nigra pars reticulata. American Epilepsy Society Annual Meeting; American Epilepsy Society; San Diego. 2006.
  • Heinemann U, Lux HD, Gutnick MJ. Extracellular free calcium and potassium during paroxsmal activity in the cerebral cortex of the cat. Exp Brain Res. 1977;27:237–243.
  • Hestrin S, Galarreta M. Electrical synapses define networks of neocortical GABAergic neurons. Trends Neurosci. 2005;28:304–309.
  • Hochman DW, Baraban SC, Owens JW, Schwartzkroin PA. Dissociation of synchronization and excitability in furosemide blockade of epileptiform activity. Science. 1995;270:99–102.
  • Hochman DW, Schwartzkroin PA. Chloride-cotransport blockade desynchronizes neuronal discharge in the “epileptic” hippocampal slice. J Neurophysiol. 2000;83:406–417.
  • Iadarola MJ, Gale K. Substantia nigra: site of anticonvulsant activity mediated by gamma-aminobutyric acid. Science. 1982;218:1237–1240.
  • Jahromi SS, Wentlandt K, Piran S, Carlen PL. Anticonvulsant actions of gap junctional blockers in an in vitro seizure model. J Neurophysiol. 2002;88:1893–1902.
  • Jenssen S, Gracely EJ, Sperling MR. How long do most seizures last? A systematic comparison of seizures recorded in the epilepsy monitoring unit. Epilepsia. 2006;47:1499–1503.
  • Jin X, Huguenard JR, Prince DA. Impaired Cl- extrusion in layer V pyramidal neurons of chronically injured epileptogenic neocortex. J Neurophysiol. 2005;93:2117–2126.
  • Jones J, Stubblefield EA, Benke TA, Staley KJ. Desynchronization of glutamate release prolongs synchronous CA3 network activity. J Neurophysiol. 2007;97:3812–3818.
  • King RD, Wiest MC, Montague PR. Extracellular calcium depletion as a mechanism of short-term synaptic depression. J Neurophysiol. 2001;85:1952–1959.
  • Kirchner A, Veliskova J, Velisek L. Differential effects of low glucose concentrations on seizures and epileptiform activity in vivo and in vitro. Eur J Neurosci. 2006;23:1512–1522.
  • Kochanek PM, Vagni VA, Janesko KL, Washington CB, Crumrine PK, Garman RH, Jenkins LW, Clark RS, Homanics GE, Dixon CE, Schnermann J, Jackson EK. Adenosine A1 receptor knockout mice develop lethal status epilepticus after experimental traumatic brain injury. J Cereb Blood Flow Metab. 2006;26:565–575.
  • Koo B. EEG changes with vagus nerve stimulation. J Clin Neurophysiol. 2001;18:434–441.
  • Kossoff EH, Ritzl EK, Politsky JM, Murro AM, Smith JR, Duckrow RB, Spencer DD, Bergey GK. Effect of an external responsive neurostimulator on seizures and electrographic discharges during subdural electrode monitoring. Epilepsia. 2004;45:1560–1567.
  • Kostopoulos G, Avoli M, Gloor P. Participation of cortical recurrent inhibition in the genesis of spike and wave discharges in feline generalized penicillin epilepsy. Brain Res. 1983;267:101–112.
  • Krahl SE, Clark KB, Smith DC, Browning RA. Locus coeruleus lesions suppress the seizure-attenuating effects of vagus nerve stimulation. Epilepsia. 1998;39:709–714.
  • Lado FA, Velisek L, Moshe SL. The effect of electrical stimulation of the subthalamic nucleus on seizures is frequency dependent. Epilepsia. 2003;44:157–164.
  • Lado FA. Chronic bilateral stimulation of the anterior thalamus of kainate-treated rats increases seizure frequency. Epilepsia. 2006;47:27–32.
  • Lin EJ, Young D, Baer K, Herzog H, During MJ. Differential actions of NPY on seizure modulation via Y1 and Y2 receptors: evidence from receptor knockout mice. Epilepsia. 2006;47:773–780.
  • Llinas R, Baker R, Sotelo C. Electrotonic coupling between neurons in cat inferior olive. J Neurophysiol. 1974;37:560–571.
  • Lothman EW, Hatlelid JM, Zorumski CF. Functional mapping of limbic seizures originating in the hippocampus: a combined 2-deoxyglucose and electrophysiologic study. Brain Res. 1985;360:92–100.
  • Ludvig N, Kuzniecky RI, Baptiste SL, John JE, von Gizycki H, Doyle WK, Devinsky O. Epidural pentobarbital delivery can prevent locally induced neocortical seizures in rats: the prospect of transmeningeal pharmacotherapy for intractable focal epilepsy. Epilepsia. 2006;47:1792–1802.
  • Lutz B. On-demand activation of the endocannabinoid system in the control of neuronal excitability and epileptiform seizures. Biochem Pharmacol. 2004;68:1691–1698.
  • MacVicar BA, Dudek FE. Local synaptic circuits in rat hippocampus: interactions between pyramidal cells. Brain Res. 1980;184:220–223.
  • Mancilla JG, Lewis TJ, Pinto DJ, Rinzel J, Connors BW. Synchronization of electrically coupled pairs of inhibitory interneurons inneocortex. J Neurosci. 2007;27:2058–2073.
  • Marrosu F, Santoni F, Puligheddu M, Barberini L, Maleci A, Ennas F, Mascia M, Zanetti G, Tuveri A, Biggio G. Increase in 20–50 Hz (gamma frequencies) power spectrum and synchronization after chronic vagal nerve stimulation. Clin Neurophysiol. 2005;116:2026–2036.
  • Marsicano G, Goodenough S, Monory K, Hermann H, Eder M, Cannich A, Azad SC, Cascio MG, Gutierrez SO, van der Stelt M, Lopez-Rodriguez ML, Casanova E, Schutz G, Zieglgansberger W, Di Marzo V, Behl C, Lutz B. CB1 cannabinoid receptors and on-demand defense against excitotoxicity. Science. 2003;302:84–88.
  • Matsumoto H, Ayala GF, Gumnit RJ. Effects of intracellularly injected currents on the PDS and the hyperpolarizing after-potential in neurons within an epileptic focus. Electroencephalogr Clin Neurophysiol. 1969;26:120.
  • McGaraughty S, Cowart M, Jarvis MF, Berman RF. Anticonvulsant and antinociceptive actions of novel adenosine kinase inhibitors. Curr Top Med Chem. 2005;5:43–58.
  • Mechoulam R, Lichtman AH. Neuroscience. Stout guards of the central nervous system. Science. 2003;302:65–67.
  • Miles R, Wong RK. Single neurones can initiate synchronized population discharge in the hippocampus. Nature. 1983;306:371–373.
  • Morris GL., 3rd A retrospective analysis of the effects of magnet-activated stimulation in conjunction with vagus nerve stimulation therapy. Epilepsy Behav. 2003;4:740–745.
  • Moshe SL, Albala BJ, Ackermann RF, Engel J., Jr Increased seizure susceptibility of the immature brain. Brain Res. 1983;283:81–85.
  • NeuroPace. Bethesda (MD): National Library of Medicine (US) 2000; 2008. . Responsive Neurostimulator (RNS™) System Long-Term Treatment Clinical Investigation. Available from: NLM Identifier: NCT00572195.
  • Nevander G, Ingvar M, Auer R, Siesjo BK. Status epilepticus in well-oxygenated rats causes neuronal necrosis. Ann Neurol. 1985;18:281–290.
  • Ochoa JG. Oral electrolyte therapy for refractory epilepsy; American Epilepsy Society Annual Meeting; San Diego. 2006.
  • Okada R, Negishi N, Nagaya H. The role of the nigrotegmental GABAergic pathway in the propagation of pentylenetetrazol-induced seizures. Brain Res. 1989;480:383–387.
  • Patrick AW, Campbell IW. Fatal hypoglycaemia in insulin-treated diabetes mellitus: clinical features and neuropathological changes. Diabet Med. 1990;7:349–354.
  • Pineau N, Charriaut-Marlangue C, Motte J, Nehlig A. Pentylene-tetrazol seizures induce cell suffering but not death in the immature rat brain. Brain Res Dev Brain Res. 1999;112:139–144.
  • Pinto DJ, Patrick SL, Huang WC, Connors BW. Initiation, propagation, and termination of epileptiform activity in rodent neocortex in vitro involve distinct mechanisms. J Neurosci. 2005;25:8131–8140.
  • Richerson GB. Looking for GABA in all the wrong places: the relevance of extrasynaptic GABA(A) receptors to epilepsy. Epilepsy Curr. 2004;4:239–242.
  • Rutecki PA, Grossman RG, Armstrong D, Irish-Loewen S. Electrophysiological connections between the hippocampus and entorhinal cortex in patients with complex partial seizures. J Neurosurg. 1989;70:667–675.
  • Schindler K, Elger CE, Lehnertz K. Increasing synchronization may promote seizure termination: evidence from status epilepticus. Clin Neurophysiol. 2007;118:1955–1968.
  • Schweitzer JS, Wang H, Xiong ZQ, Stringer JL. pH Sensitivity of non-synaptic field bursts in the dentate gyrus. J Neurophysiol. 2000;84:927–933.
  • Schwindt PC, Spain WJ, Crill WE. Long-lasting reduction of excitability by a sodium-dependent potassium current in cat neocortical neurons. J Neurophysiol. 1989;61:233–244.
  • Shehab S, Simkins M, Dean P, Redgrave P. The dorsal midbrain anticonvulsant zone-III. Effects of efferent pathway transections on suppression of electroshock seizures and defence-like reactions produced by local injections of bicuculline. Neuroscience. 1995;65:697–708.
  • Shehab SA, Ljubisavljevic M, Al-Halhali F, Al-Awadhi A, Madathil M, Abdul-Kareem A, Redgrave P. Experimental manipulations of the subthalamic nucleus fail to suppress tonic seizures in the electroshock model of epilepsy. Exp Brain Res. 2006;173:274–281.
  • Shinnar S, Berg AT, Moshe SL, Shinnar R. How long do new-onset seizures in children last? Ann Neurol. 2001;49:659–664.
  • Sperber EF, Wurpel JN, Moshe SL. Evidence for the involvement of nigral GABAB receptors in seizures of rat pups. Brain Res Dev Brain Res. 1989;47:143–146.
  • Sperber EF, Veliskova J, Germano IM, Friedman LK, Moshe SL. Age-dependent vulnerability to seizures. Adv Neurol. 1999;79:161–169.
  • Spray DC, Harris AL, Bennett MV. Gap junctional conductance is a simple and sensitive function of intracellular pH. Science. 1981;211:712–715.
  • Staley KJ, Longacher M, Bains JS, Yee A. Presynaptic modulation of CA3 network activity. Nat Neurosci. 1998;1:201–209.
  • Stell BM, Brickley SG, Tang CY, Farrant M, Mody I. Neuroactive steroids reduce neuronal excitability by selectively enhancing tonic inhibition mediated by delta subunit-containing GABAA receptors. Proc Natl Acad Sci U S A. 2003;100:14439–14444.
  • Swadlow HA. Fast-spike interneurons and feedforward inhibition in awake sensory neocortex. Cereb Cortex. 2003;13:25–32.
  • Szente M, Gajda Z, Said Ali K, Hermesz E. Involvement of electrical coupling in the in vivo ictal epileptiform activity induced by 4-aminopyridine in the neocortex. Neuroscience. 2002;115:1067–1078.
  • Thimm J, Mechler A, Lin H, Rhee S, Lal R. Calcium-dependent open/closed conformations and interfacial energy maps of reconstituted hemichannels. J Biol Chem. 2005;280:10646–10654.
  • Thiry A, Dogne JM, Supuran CT, Masereel B. Carbonic anhydrase inhibitors as anticonvulsant agents. Curr Top Med Chem. 2007;7:855–864.
  • Tian GF, Azmi H, Takano T, Xu Q, Peng W, Lin J, Oberheim N, Lou N, Wang X, Zielke HR, Kang J, Nedergaard M. An astrocytic basis of epilepsy. Nat Med. 2005;11:973–981.
  • Timofeev I, Grenier F, Steriade M. Contribution of intrinsic neuronal factors in the generation of cortically driven electrographic seizures. J Neurophysiol. 2004;92:1133–1143.
  • Timofeev I, Steriade M. Neocortical seizures: initiation, development and cessation. Neuroscience. 2004;123:299–336.
  • Traub RD, Draguhn A, Whittington MA, Baldeweg T, Bibbig A, Buhl EH, Schmitz D. Axonal gap junctions between principal neurons: a novel source of network oscillations, and perhaps epileptogenesis. Rev Neurosci. 2002;13:1–30.
  • Traub RD, Michelson-Law H, Bibbig AE, Buhl EH, Whittington MA. Gap junctions, fast oscillations and the initiation of seizures. Adv Exp Med Biol. 2004;548:110–122.
  • Trevelyan AJ, Sussillo D, Yuste R. Feedforward inhibition contributes to the control of epileptiform propagation speed. J Neurosci. 2007;27:3383–3387.
  • Trexler EB, Bukauskas FF, Bennett MV, Bargiello TA, Verselis VK. Rapid and direct effects of pH on connexins revealed by the connexin46 hemichannel preparation. J Gen Physiol. 1999;113:721–742.
  • Valiunas V. Biophysical properties of connexin-45 gap junction hemichannels studied in vertebrate cells. J Gen Physiol. 2002;119:147–164.
  • Velisek L, Moshe SL, Xu SG, Cammer W. Reduced susceptibility to seizures in carbonic anhydrase II deficient mutant mice. Epilepsy Res. 1993;14:115–121.
  • Velisek L, Dreier JP, Stanton PK, Heinemann U, Moshe SL. Lowering of extracellular pH suppresses low-Mg(2+)-induces seizures in combined entorhinal cortex-hippocampal slices. Exp Brain Res. 1994;101:44–52.
  • Velisek L. Extracellular acidosis and high levels of carbon dioxide suppress synaptic transmission and prevent the induction of long-term potentiation in the CA1 region of rat hippocampal slices. Hippocampus. 1998;8:24–32.
  • Veliskova J, Velsek L, Moshe SL. Subthalamic nucleus: a new anticonvulsant site in the brain. Neuroreport. 1996;7:1786–1788.
  • Veliskova J, Kubova H, Friedman LK, Wu R, Sperber EF, Zukin RS, Moshe SL. The expression of GABA(A) receptor subunits in the substantia nigra is developmentally regulated and region-specific. Ital J Neurol Sci. 1998;19:205–210.
  • Veliskova J, Moshe SL. Sexual dimorphism and developmental regulation of substantia nigra function. Ann Neurol. 2001;50:596–601.
  • Veliskova J, Miller AM, Nunes ML, Brown LL. Regional neural activity within the substantia nigra during peri-ictal flurothyl generalized seizure stages. Neurobiol Dis. 2005;20:752–759.
  • Veliskova J, Moshe SL. Update on the role of substantia nigra pars reticulata in the regulation of seizures. Epilepsy Curr. 2006;6:83–87.
  • Vergnes M, Boehrer A, Simler S, Bernasconi R, Marescaux C. Opposite effects of GABAB receptor antagonists on absences and convulsive seizures. Eur J Pharmacol. 1997;332:245–255.
  • Vezzani A, Sperk G, Colmers WF. Neuropeptide Y: emerging evidence for a functional role in seizure modulation. Trends Neurosci. 1999;22:25–30.
  • Vezzani A, Michalkiewicz M, Michalkiewicz T, Moneta D, Ravizza T, Richichi C, Aliprandi M, Mule F, Pirona L, Gobbi M, Schwarzer C, Sperk G. Seizure susceptibility and epileptogenesis are decreased in transgenic rats overexpressing neuropeptide Y. Neuroscience. 2002;110:237–243.
  • Vezzani A, Sperk G. Overexpression of NPY and Y2 receptors in epileptic brain tissue: an endogenous neuroprotective mechanism in temporal lobe epilepsy? Neuropeptides. 2004;38:245–252.
  • Wallace MJ, Blair RE, Falenski KW, Martin BR, DeLorenzo RJ. The endogenous cannabinoid system regulates seizure frequency and duration in a model of temporal lobe epilepsy. J Pharmacol Exp Ther. 2003;307:129–137.
  • Yamada K, Ji JJ, Yuan H, Miki T, Sato S, Horimoto N, Shimizu T, Seino S, Inagaki N. Protective role of ATP-sensitive potassium channels in hypoxia-induced generalized seizure. Science. 2001;292:1543–1546.
  • Young D, Dragunow M. Status epilepticus may be caused by loss of adenosine anticonvulsant mechanisms. Neuroscience. 1994;58:245–261.
  • Zivanovic D, Bernaskova K, Kaminskij Y, Mares P. Action of GABA-B antagonist on cortical epileptic afterdischarges in rats is similar to that of GABA-A antagonist. Physiol Res. 2003;52:651–655.

Unfortunately, for people who do not respond to existing drugs, new ones that might help will not be coming soon. “There aren’t any major drugs in the pipeline at the moment,” Rogawski says. A 2013 joint report from epilepsy research organizations explained that “because the marketplace is already awash with , many pharmaceutical companies now refrain from the expensive enterprise of developing new compounds.”

Faced with this roadblock, many patients and families have opted to conduct their own experiments. In recent years, for example, as marijuana was approved for medical uses in Colorado and other states, parents of children with Dravet syndrome have started giving their sons and daughters doses of cannabidiol, a nonpsychoactive component of the plant, prepared as an oil. In anecdotal reports online and in the media, some families described a dramatic reduction in seizures. Since then, a few clinical studies of cannabidiol have also supported its potential as an effective treatment for some forms of epilepsy.

In 2014 GW Pharmaceuticals, a British drug company, received special permission from the U.S. Food and Drug Administration to test its pharmaceutical version of cannabidiol, called Epidiolex. In a recent trial of 225 patients, completed in September 2016, participants who took the drug (along with their other epilepsy medications) reduced their nonstop seizures by 42 percent, compared with 17 percent for those taking a placebo.

Other groups have taken a page from history to develop a nutritional approach to treating epilepsy. A so-called ketogenic diet (high in fats and low in carbohydrates) was widely used in the 1920s to lessen seizures, particularly in children. Recent studies have confirmed that it offers some antiseizure benefits, although 90 percent of children in one study found the diet so unpalatable that they eventually dropped it.

Given how long it is likely to take for new medications against epilepsy to be tested and approved, some experts argue that more patients with relentless epilepsy could benefit from recent advances in surgical techniques and various methods for stimulating neurons in ways that make them behave less erratically. Devinsky estimates that up to 20 percent of such patients are candidates for surgery because they have focal seizures that can be traced to a specific and surgically approachable site in the brain.

Another option that has been around for two decades consists of a kind of pacemaker for the brain. The idea is to prevent seizures by stimulating the vagus nerve in the neck, via electrodes attached to a battery pack implanted in the chest. A programmed pattern of mild electric current overrides and calms the abnormal activity in the brain. A 2011 meta-analysis of 74 clinical trials involving more than 3,300 subjects found that vagus nerve stimulation reduced seizures by more than half in 50 percent of the patients.

A newer device, NeuroPace’s RNS System, approved by the FDA in 2013, has a neurostimulator that is implanted in the skull, under the scalp. When it detects unusual electrical activity in the brain, it sends a charge through two electrodes to stop or even prevent a seizure. According to Devinsky, 10 to 15 percent of patients with otherwise unmanageable epilepsy are potential candidates for the treatment; clinical trials have shown that the implants reduce seizures in the treated group by an average of as much as 66 percent after three to six years of follow-up.

In the laboratory, meanwhile, researchers are working with mice, fruit flies, worms and computers to develop new and better models of epilepsy in animals, in an effort to speed drug discovery. In 2016, for example, scientists at Florida Atlantic University and the Scripps Research Institute for the first time induced seizures in nematodes, microscopic worms with just 302 brain cells. They then successfully treated the creatures with existing antiepileptic drugs, suggesting the worms could potentially serve as fast and efficient tools for testing new medicines.

As for Richard Shane, who now owns his own travel company, epilepsy is still part of his life. He no longer has seizures, but there is something else that nags at him: “I wonder sometimes who I would have been if I never had all this electrical activity in my brain. How did it change who I am?”

It is a question without an answer, another unknown in the swirl of unknowns around drug-resistant epilepsy. But doctors such as Gregory Bergey, director of the Johns Hopkins Epilepsy Center, try to offer encouragement as they confront the disorder’s myriad riddles: “I always tell my patients, we never give up.”

Epilepsy is a chronic neurological disease characterized by recurrent, unprovoked seizures caused by a disruption of electrical surges in the brain, according to the Epilepsy Foundation. The fourth most common neurological disorder in America, epilepsy is most often diagnosed in childhood or after the age of 65 but can occur in anyone at any age.

Seizures can last from a few seconds to a few minutes, and sometimes it’s hard to tell that a person is having one, according to the Centers for Disease Control and Prevention.

Seizure signs and symptoms may include:

  • Temporary confusion—often described as a “fuzzy” feeling
  • A staring spell
  • Uncontrollable jerking movements of the arms and legs
  • Loss of consciousness or awareness
  • Psychic symptoms—out-of-body feelings or not feeling “in the moment”
  • Memory lapses

In most cases, a person with epilepsy will tend to have the same type of seizure each time, so symptoms will be similar from episode to episode.

Treating epilepsy

Some treatments work better than others, depending on the type of epilepsy diagnosed. Treatment options include anti-seizure medication, surgery, nerve stimulation, and diet changes. The goal of treatment is to achieve no seizures and no side effects, enabling those who have epilepsy to live independently.

While many internists and family practice doctors treat epilepsy, a neurologist—a doctor who specializes in the brain and nervous system—typically is best able to diagnose and treat epilepsy. Some cases are difficult to treat, and those patients often consult with an epileptologist, a neurologist who specializes in epilepsy treatment.

Seizure warning signs

Many people experience an aura before having a seizure. It is kind of the body’s way of warning them that a seizure is headed their way.

Common warning signs of seizures include:

  • Sensitivity to smells, sounds, or sights
  • Anxiety
  • Nausea
  • Dizziness
  • Visual changes, such as tunnel vision

Keeping a journal of what’s triggered seizures and what warning signs occurred before they happened can help epilepsy sufferers better control their seizures.

What can trigger an epileptic seizure?

People with epilepsy report a variety of things that can trigger a seizure. They include:

  • Stress
  • Missing medication
  • Lack of sleep
  • Fever
  • Flashing lights
  • Alcohol, drugs, and caffeine
  • Nicotine
  • Low blood sugar

Not all seizures are emergencies. To help someone having a seizure, focus on safety. Give the person room, clear hard or sharp objects, and cushion the head. Don’t try to hold the person down, stop movements, or put anything in the person’s mouth. For milder seizures, like ones involving staring or shaking arms or legs, guide the person away from hazards—sharp objects, traffic, stairs. Don’t leave someone who’s had a seizure alone. Stay until the person is aware of where he or she is and responds normally when spoken to. Keep track of how long the seizure lasts. The CDC recommends calling 911 if a seizure lasts more than five minutes or if the person gets injured during the seizure.

What causes epileptic seizures?

While one in 26 people will develop epilepsy, more than half of the time its cause is unknown, according to the Epilepsy Foundation.

The known causes include:

  • Traumatic brain injury
  • Neurologic diseases, such as Alzheimer’s
  • Stroke
  • Brain tumor
  • Brain infection, such as meningitis
  • Loss of oxygen to the brain
  • Some genetic disorders, such as Down syndrome

Classifying seizures

There are three major groups of seizures—generalized onset, focal onset, and unknown onset—and a lengthy breakdown of specific symptoms under each category. The differences among the types are in how and where they begin in the brain.

Generalized seizures affect both sides of the brain, focal onset seizures start in one area on one side of the brain, and the unknown label categorizes seizures when the beginning can’t be determined.

Diagnosing epilepsy

Experts recommend anyone who experiences seizure symptoms should seek medical advice because epilepsy can be diagnosed only by a medical professional. Many people who have seizures take tests such as an electroencephalogram—an EEG—which can show which parts of the brain are not behaving normally. According to the International League Against Epilepsy, patients are diagnosed with epilepsy if they have two unprovoked seizures more than 24 hours apart or one unprovoked seizure and a high risk of having another.

Do’s and Don’ts of Seizures

Plus, 6 Things to Know About Epilepsy

Epilepsy, also called seizure disorder, is a disease of the brain that causes recurrent, unprovoked seizures. Epilepsy disrupts the brain’s normal electrical functions with abnormal bursts of electrical energy.

Although epilepsy is the fourth most common neurological disease, it can sometimes be difficult to diagnose. Epilepsy can be caused by a variety of factors, from genetics to structural changes in the brain. Your care team will work with you to determine the cause and best treatment options.

Whether you or a loved one has epilepsy, here are six things you should know.

1. Epilepsy affects people of all ages.

Epilepsy and seizures can develop at any point in someone’s lifetime. In fact, one in 26 people will develop epilepsy. New cases are most common with younger children, particularly in the first year of life. However, cases also increase after age 55, as individuals develop strokes, brain tumors and Alzheimer’s disease.

2. Seizures are different in everyone.

Each person’s seizure is different. Some can last a few seconds while others can last minutes. It’s important to know that some seizures will have other symptoms, such as numbness, impaired speech and sudden confusion.

Although every seizure is different, there are two main types, defined by the location of impact in the brain:

  • A partial (focal) seizure occurs in a limited area of the brain. This type is responsible for approximately 60% of seizures. The person having the seizure will not remember it. They may appear to be twitching their arms. Other symptoms can include tingling, numbness, unusual head movements, flushed face or nausea.
  • A generalized seizure affects both hemispheres of the brain at once. The generalized tonic-clonic seizure, also known as a grand mal seizure, is part of this group. In this type of seizure, the person will undergo three stages. First, the person will become unresponsive. They will enter a tonic phase, which results in stiffened limbs. The clonic phase results in jerking limbs. Eventually, the jerking will stop and the person will regain consciousness. Full recovery after this type of seizure can take minutes to hours.

In addition to grand mal seizures, generalized seizures also include absence (or petit mal) seizures, the most common seizure in children under 14. In these seizures, the person may become unresponsive and appear to be staring ahead. Their eyes may even roll into the back of their head. These types of seizures only last a few seconds. They may also be accompanied by chewing movements or excessive blinking.

If your loved one exhibits any signs of seizure, record as much information as you can.

3. It’s important to know how to provide first aid to someone experiencing a seizure.

Some seizures are more dangerous than others. While there isn’t much you can do during a seizure to stop it, you can help protect the individual and provide assistance. Nineteen out of 20 seizures stop by themselves within two to three minutes, although there can be a prolonged period of confusion afterwards. For seizures that last longer than five minutes, a call for an ambulance should be placed.

First, remember to remain calm. If appropriate, lay the individual on their side or cushion their head with a pillow. Once they are protected, call for help and remain with them until they recover. During the seizure, you should never put anything in the person’s mouth. This could cause serious injury. Here are some other things to be mindful of during a seizure.

Things to DO:

  • Do call for emergency assistance when needed.
  • Do safely cushion the person’s head.
  • Do protect the person from any nearby objects.
  • Do time the length of the seizure.
  • Do stay with the person until they recover.

Things you should NOT DO:

  • Don’t put anything in the person’s mouth.
  • Don’t try to move the person.
  • Don’t try to restrain the person.

4. Women with epilepsy can give birth to healthy babies.

Women with epilepsy can have perfectly healthy pregnancies. If possible, plan your pregnancy so you know the cause of your seizures and safest seizure medication to treat them during a pregnancy. Work with your care team before, during and after your pregnancy. Continue taking your medication as prescribed until you consult with your physician. Be sure to discuss all seizure medications with your care team to determine the best care for you. You will also want to be mindful of avoiding any triggers, such as sleep deprivation, certain foods or stress.

5. Medication can control epilepsy and allow people to live full lives.

Epilepsy is common! More than 3 million people in the United States have epilepsy. With the proper medication and treatment, people with epilepsy can have reduced symptoms, and live full and active lives. A multidisciplinary approach, like the one at Northwestern Medicine Comprehensive Epilepsy Center, can help you navigate your disease and maximize quality of life.

6. If medication is not effective, minimally invasive surgery may be an option.

For patients who cannot be controlled with medication, surgery is usually the best chance to stop the seizures in the right candidates. Roughly 20% of patients who previously were not considered candidates for surgery may now be helped through minimally invasive techniques. Stereo EEG can pinpoint the onset of the seizures, and laser ablation may be able to destroy the small brain part causing the seizures without requiring major surgery. Another promising advancement in epilepsy care is the use of a responsive neurostimulator (RNS), which acts like a cardiac pacemaker, but in the brain. The RNS is attached to the brain tissue where seizures originate, and when it detects an abnormal electrical impulse leading up to a seizure, it provides a pulse of electricity that can prevent the patient from ultimately having a seizure.

About the author

Leave a Reply

Your email address will not be published. Required fields are marked *