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Human brain lobes, beautiful colorful illustration detailed anatomy. Sagittal view of the brain. Isolated on a white background.

Seizures (also called “fits” or convulsions) are episodes of disturbed brain function that cause changes in attention or behavior. They are caused by abnormally excited electrical signals in the brain. There are a number of different types of seizures, including

  • Absence (petit mal) seizure
  • Generalized tonic-clonic (grand mal) seizure
  • Partial (focal) seizure

Epilepsy is a brain disorder involving repeated, spontaneous seizures of any type.

The severity of symptoms can vary greatly, from simple staring spells to loss of consciousness and violent convulsions.

More . . .

For most people with epilepsy, each seizure is similar to previous ones. The type of seizure a person has depends on a variety of things, such as the part of the brain affected and the underlying cause of the seizure. An aura consisting of a strange sensation (such as tingling, smelling an odor that isn’t actually there, or emotional changes) occurs in some people prior to each seizure.







Sometimes a seizure is related to a temporary condition, such as exposure to drugs, withdrawal from certain drugs, a high fever, or abnormal levels of sodium or glucose in the blood. If the seizure or seizures do not happen again once the underlying problem is corrected, the person does NOT have epilepsy.

In other cases, permanent injury to or changes in brain tissue cause the brain to be abnormally excitable. In these cases, the seizures happen without an immediate cause. This is epilepsy. Epilepsy can affect people of any age.

Epilepsy may be idiopathic, which means the cause cannot be identified. These seizures usually begin between ages 5 and 20, but they can happen at any age. People with this condition have no other neurological problems, but sometimes have a family history of seizures or epilepsy.

The Studies


The studies listed below are organized by date, with the most recent date first.  Some of the full texts will need a password because they are kept in a locked file to protect their copyright.  For educational purposes only, we are allowed to share the password with you if you write to us.

If you are trying to find a particular author, see the Index below which lists all the primary authors alphabetically with their publication dates.

Author Index
  1. Chen 1980
  2. Chen 1980
  3. Cysneiros 2009
  4. Egger 1985
  5. Egger 1989
  6. Kaczorowska 2008
  7. Koppel 1991
  8. Lopes 2013
  9. Scorza 2009
  10. Scorza 2010
  11. Struys 2012
  12. Yoon 2014
Yoon 2014: PUFA (Omega-3) in ketogenic diet

Polyunsaturated fatty acid-enriched diet therapy for a child with epilepsy, Yoon JR, Lee EJ, Kim HD, Lee JH, Kang HC, Brain & Development, 2014 Feb;36(2):163-6

The ketogenic diet (KD) is a high-fat, low-carbohydrate diet with an established efficacy for treating medically refractoryepilepsy in children. Fatty acids are the most important constituent of the KD in all aspects of efficacy and complications. Among fatty acids, polyunsaturated fatty acids (PUFAs) increase anticonvulsant properties and reduce the complications associated with the high-fat diet. Here, we report a 7-year-old boy with Lennox-Gastaut syndrome combined with mitochondrial respiratory chain complex I deficiency, whose medically intractable seizures have been successfully controlled with a PUFA-enriched modified Atkins diet without any significant adverse events. The diet consists of canola oil and diverse menu items like fish and nuts instead of olive oil and has an ideal 1:2.8 ratio of omega-3 to omega-6. In addition, fractionation of this boy’s plasma showed normal levels of fatty acids, including omega-3 (alpha-linoleic acid, eicosapentaenoic acid) and omega-6 (linoleic acid, arachidonic acid) as well as monounsaturated fatty acids (oleic acid). Plasma docosahexanoic acid remained low after PUFA-enriched diet therapy. PUFA-enriched diet therapy is likely to increase the efficacy of diet therapy and reduce complications of a high-fat diet in children with refractory epilepsy.

MedLine || Full Text

Lopes 2013: Omega-3 reduces heart rate in epilepsy

Omega-3 fatty acid supplementation reduces resting heart rate of rats with epilepsy., Lopes MD1, Colugnati DB, Lopes AC, Scorza CA, Cavalheiro EA, Cysneiros RM, Scorza FA., Epilepsy & Behavior, 2013 Jun;27(3):504-6

Since cardiovascular dysfunction may contribute to sudden unexpected death in epilepsy (SUDEP), the consumption of omega-3 fatty acids (omega-3 FAs) might be beneficial as an adjunctive therapy for SUDEP prevention. It is well recognized that omega-3 FAs exert positive effects on the cardiovascular system including heart rate (HR) reduction, a major risk factor to sudden death. Thus, we evaluated the effects of chronic supplementation of omega-3 FAs on the HR of rats with epilepsy. In agreement with our previous investigations, this study also showed that the HR of animals with epilepsy is higher than that of the control group. Quite interestingly, chronic supplementation with omega-3 FAs restored the HR of rats with epilepsy toward control values. In conclusion, although further investigations are still required, our preliminary results showed a potential preventive effect of omega-3 FA supplementation against SUDEP

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Struys 2012: Case studies on Vitamin B6 dependent epilepsy

Pyridoxine-dependent epilepsy with elevated urinary α-amino adipic semialdehyde in molybdenum cofactor deficiency,  Struys EA1, Nota B, Bakkali A, Al Shahwan S, Salomons GS, Tabarki B.,  Pediatrics. 2012 Dec;130(6):e1716-9.

α-Amino adipic semialdehyde (α-AASA) accumulates in body fluids from patients with pyridoxine-dependent epilepsy because of mutations in antiquitin (ALDH7A1) and serves as the biomarker for this condition. We have recently found that the urinary excretion of α-AASA was also increased in molybdenum cofactor and sulfite oxidase deficiencies. The seizures in pyridoxine-dependent epilepsy are caused by lowered cerebral levels of pyridoxal-5-phosphate (PLP), the bioactive form of pyridoxine (vitamin B(6)), which can be corrected by the supplementation of pyridoxine. The nonenzymatic trapping of PLP by the cyclic form of α-AASA is causative for the lowered cerebral PLP levels. We describe 2 siblings with clinically evident pyridoxine-responsive seizures associated with increased urinary excretion of α-AASA. Subsequent metabolic investigations revealed several metabolic abnormities, all indicative for molybdenum cofactor deficiency. Molecular investigations indeed revealed a known homozygous mutation in the MOCS2 gene. Based upon the clinically evident pyridoxine-responsive seizures in these 2 siblings, we recommend considering pyridoxine supplementation to patients affected with molybdenum cofactor or sulfite oxidase deficiencies.

MedLine || Full Text

Scorza 2010: Fish is good but mercury is bad in epilepsy

Fish consumption, contaminants and sudden unexpected death in epilepsy: many more benefits than risks.  Scorza FA1, Cysneiros RM, Arida RM, Terra VC, Machado HR, Rabello GM, Albuquerque M, Cavalheiro EA., Brazilian Journal of Biology, 2010 Aug;70(3):665-70.

People with epilepsy have an increased risk of dying prematurely and the most common epilepsy-related category of death is sudden unexpected death in epilepsy (SUDEP). SUDEP is mainly a problem for patients with chronic uncontrolled epilepsy. The ultimate goal of research in SUDEP is to develop new methods to prevent it and actions other than medical and surgical therapies that could be very useful. Nutritional aspects, i.e., omega-3 fatty acids deficiency, could have an interesting role in this scenario. Some animal and clinical studies have suggested that omega-3 fatty acids could be useful in the prevention and treatment of epilepsy and hence SUDEP. It has been ascertained that the only foods that provide large amounts of omega-3 are seafood (fish and shellfish); however, some fish are contaminated with methylmercury, which may counteract the positive effects of omega-3 fatty acids. Our update review summarises the knowledge of the role of fish consumption on epilepsy research.

MedLine || Full Text

Scorza 2009: Rat study on alcohol and epilepsy

Alcohol consumption and sudden unexpected death in epilepsy: experimental approach.
Scorzai CA1, Cysneiros RM, Arida RM, Terra VC, Machado HR, de Almeida AC, Cavalheiro EA, Scorza FA.,  Arquivos de Neuro-Psiquiatria. 2009 Dec;67(4):1003-6.

… In B group (drinking alcohol), it was observed a significant seizure increase (11.6+/-5.3) during the first 2 weeks of alcohol administration and quite interesting, one rat died suddenly after a generalized tonic-clonic seizure during this period. We concluded in our experimental study that exist a possible association between alcohol abuse and SUDEP (sudden unexpected death in epilepsy) occurrence.

MedLine || Full Text



Cysneiros 2009: Omega 3 for epilepsy

Epilepsy and sudden unexpected death in epilepsy?: eat more fish! A group hypothesis.
Cysneiros RM1, Terra VC, Machado HR, Arida RM, Albuquerque Md, Scorza CA, Cavalheiro EA, Scorza FA., Arqivo de Neuro-Psiquiatria,  2009 Sep;67(3B):927-9.

Epilepsy is the commonest serious neurological disorder and individuals with epilepsy are at higher risk of death than the general population and sudden unexpected death in epilepsy (SUDEP) is the most important direct epilepsy-related cause of death. Potential pathomechanisms for SUDEP are unknown, but it is very probable that cardiac arrhythmias during and between seizures play a potential role. The ultimate goal of SUDEP research is to develop methods to prevent it and nutritional aspects such as omega-3 fatty acid deficiency may have an interesting role in this scenario. Omega-3 fatty acids reduce the risk of cardiovascular mortality and are important for treating or preventing some neurological diseases, including epilepsy. A dietary modification or nutritional supplements increasing the ingestion of omega-3 fatty acids may help to ”save the brain’.

MedLine || Full Text 

Kaczorowska 2008: Vitamin B6 and seizures

Pyridoxine-dependent seizures caused by alpha amino adipic semialdehyde dehydrogenase deficiency: The first Polish case with confirmed biochemical and molecular pathology, Kaczorowska M1, Kmiec T, Jakobs C, Kacinski M, Kroczka S, Salomons GS, Struys EA, Jozwiak S., Journal of Child Neurology, 2008 Dec;23(12):1455-9

Pyridoxine [vitamin B6] dependent seizures are a rare condition recognized when numerous seizures respond to pyridoxine treatment and recur on pyridoxine withdrawal. For decades the diagnosis was confirmed only with pyridoxine treatment withdrawal trial. Recently described biochemical and molecular pathology improved the diagnostic process for those cases in which seizures are caused by alpha amino adipic semialdehyde dehydrogenase deficiency. This article presents a girl with recurrent status epilepticus episodes resistant to phenobarbital and phenytoin and partly responding to midazolam. Eventually the seizures were completely controlled with pyridoxine; however, due to the severe condition of this child when seizing, no trial of withdrawal has been performed. The diagnosis of pyridoxine-dependent seizures was confirmed with biochemical and molecular testing revealing elevated alpha-AASA excretion and the presence of 2 different mutations in the antiquitin ( ALDH7A1) gene. Due to the availability of reliable laboratory testing, confirmation of the diagnosis was made without the life-threatening trial of pyridoxine withdrawal.

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Koppel 1991: Allergy to dye in seizure meds

Tegretol excipient-induced allergy, Koppel BS, Harden CL, Daras M., Archives of Neurology, 1991 Aug;48(8):789.

To the Editor.  —Allergies to drugs are usually caused by the active ingredient. However, inert excipients (coloring agents, preservatives, and sweeteners) may also sometimes cause allergic reactions.1-4 The incidence of these may be increasing, because excipients are now usually chemically produced synthetics, not naturally derived substances. We report a patient with epilepsy who developed sensitivity to FD&C Red 40 in the Tegretol brand of carbamazepine.

Report of a Case.  —A 56-year-old woman had had frequent complex partial and rare secondarily generalized seizures for 5 years. Control was poor with therapeutic plasma levels of phenytoin, primidone, and phenobarbital. Treatment with the Tegretol brand of carbamazepine (Ciba-Geigy) was started, and other drugs were withdrawn. Four weeks later, she complained of rhinorrhea, tearing, and nasal stuffiness that consistently occurred within 20 minutes after ingesting a Tegretol tablet. Generic carbamazepine (a white tablet made by Bioline MAF) was substituted at the same dose,

MedLine || Full Text

Egger 1989: Double-blind study on children with ADHD/ migraine/ GI pain & seizures

Oligoantigenic diet treatment of children with epilepsy and migraine, Egger J, Carter CM, Soothill JF, Wilson J, Journal of Pediatrics 1989 Jan;114(1):51-8.

Of 45 children with epilepsy and recurrent headaches, abdominal symptoms, or hyperkinetic behavior [old name for ADHD], 36 [80%] improved on an oligoantigenic diet . . . “Headaches, abdominal pains, and hyperkinetic behavior ceased in all those whose seizures ceased, and in some of those whose seizures did not cease.” . . . “Of 24 children with generalized epilepsy, 18 [75%] recovered or improved (including 4 of 7 with myoclonic seizures and all with petit mal), as did 18 of 21 [85%] children with partial epilepsy. In double-blind, placebo-controlled provocation studies, symptoms recurred in 15 of 16 children, including seizures in eight; none recurred when placebo was given. Eighteen other children, who had epilepsy alone, were similarly treated with an oligoantigenic diet; none improved.”
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Egger 1985: Controlled trial of diet in ADHD (& headache, GI pain, seizures)


Controlled Trial of Oligoantigenic Treatment in the Hyperkinetic Syndrome, J.Egger, P.J.Graham, J.F.Soothill, C.M.Carter, D.Gumley, The Lancet, March 9, 1985

62 of 76 selected overactive children (81.6%) improved; other symptoms such as headaches, abdominal pain, and fits, also improved.
MedLine || Full Text || Get Password

Chen 1980: Salicylates make mouse more vulnerable to seizures

Potentiation of acoustic-trauma-induced audiogenic seizure susceptibility by salicylates in mice. Chen CS, Aberdeen GC, Experientia 1980 Mar 15;36(3):330-1

Combined exposure to noise and salicylates was found to produce greater acoustic trauma induced audiogenic seizure risk than exposure to the noise alone. The result suggests that salicylates could make the mouse cochlea more vulnerable to the traumatic action of noise.


Chen 1980: Salicylates make seizure-resistant mice vulnerable to seizures

Potentiation of noise-induced audiogenic seizure risk by salicylate in mice as a function of salicylate-noise exposure interval, Chen CS, Aberdeen GC, Acta Otolaryngol 1980;90(1-2):61-5

” Audiogenic seizure risk can be induced in genetically seizure-resistant BALB/c mice by exposure to an intense noise. . . . the greatest potentiation effect was obtained when animals were exposed to the noise 6 hr after the intake of salicylate. The findings were taken as indirect evidence suggesting that the ototoxic action of sodium salicylate could potentiate vulnerability of the mouse cochlea to noise damage.”


The Diet Connection

Chen in 1980 caused seizures in seizure-resistant mice by first exposing them to salicylate and then 6 hours later to a loud noise.

A number of studies by Egger in the 1980s and 1990s have shown that many symptoms including “fits” improved or resolved on an oligoantigenic (few foods) diet similar to the Feingold diet. Cysneiros et al published a review in 2009 suggesting that increased omega 3 (as in fish oil) could help prevent sudden death from epilepsy, as well as improving the condition itself.

We recall one member who reported her son’s seizures were not controlled by the medication he was on until she also put him on the Stage One Feingold diet. For him, the combination finally controlled his seizures.

The Ketogenic diet has been used for many years to control seizures that would not respond to the usual medications. This is not a do-it-yourself diet like the Feingold diet, but must be implemented with careful medical supervision. You can get more information about it at the Charlie Foundation.  Meryl Streep also starred in an excellent film on the subject called “First Do No Harm” which is available at the Charlie Foundation website.

Click on picture to enlarge

Lau 2006; Click on picture to enlarge

In 2006, Lau published a toxicology study on combinations of synthetic colorings plus other additives (MSG and aspartame). She found that not only was each additive alone toxic to neurites (the little spiky axons and dendrites growing out of the neuron or nerve cell) but that when tested together, in amounts likely to be found in an ordinary snack, they were many times more toxic.

A diet free of synthetic additives is good for everybody, but it’s probably even more important for the person dealing with neurological disorders.

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