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What Causes Epilepsy? From GABA to Zinc

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Biology 202
1999 Final Web Reports
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What Causes Epilepsy? From GABA to Zinc

Carly Cenedella

Epilepsy is "a diverse collection of disorders" (1). In the United States, there are close to one million people with epilepsy-- about 1 in 200 people around the world have epilepsy(3). This is a review of the emerging insights into the mechanisms underlying the most common form of epilepsy, complex partial epilepsy(1).

Terminology and Classification of Epileptic Seizures

The term seizure refers to a transient alteration of behavior due to abnormal synchronized and repetitive bursts of firing of neurons in the central nervous system. Epilepsy is syndrome of episodic brain dysfunction characterized by recurrent unpredictable spontaneous seizures. Partial seizures begin in a localized brain region, whereas generalized seizures show widespread involvement of both hemispheres. Examples of generalized seizures are absences (petit mal), myoclonic, or tonic-clonic (grand mal) seizures. A complex partial seizure is associated with impairment of consciousness while a simple partial seizure is not. Most complex partial seizures originate from the temporal lobe and are also called temporal lobe seizures. Epileptics frequently have more than one type of seizure. When simple partial seizure precedes a complex partial seizure, it is referred to as an aura. More recent classifications of epileptic syndromes incorporate such features as etiology, age of onset, and the different combinations of seizures that an epileptic has. Other commonly used terms include ictal (of seizure itself) and interictal (between seizures). Convulsion implies ictal behavior with vigorous motor activities. Status epilepticus denotes a very prolonged seizure or series of seizures occurring so frequently that full recovery of brain function does not occur interictally (1).

Complex partial seizures constitute a major percentage of epilepsies and as a result of impaired consciousness are rather disabling. They are often medically intractable in that the administration of medication will not control the seizures. Most cases of complex partial epilepsy appear to stem from an abnormality in the temporal lobe, since partial resection of the temporal lobe, including the mesial structures, hippocampus, and amygdala, virtually eliminates seizures in more than 80% of selected patients. Examination of tissues of the surgical specimens and autopsy studies of patients with chronic temporal lobe epilepsy most often reveal sclerosis of the hippocampus, termed Ammons horn sclerosis, which is characterized by a marked loss of the principal neurons of hippocampus (1).

Jackson and his Early Theory on Epilepsy and Brain Organization

In the 1800s, it was noted by Jackson that epileptic seizures begin in isolated parts of the body such as the thumb and from there spread to neighboring regions perhaps the arm and then to the rest of the body. He hypothesized that there were areas in cerebral cortex that controlled isolated movements and that the areas that were adjacent in the brain were anatomically adjacent as well. Therefore, a seizure began in one area and spread to the rest of the cortex. His hypothesis was later substantiated by Fritsch and Hittig's excitation experiments on motor cortex or area 4. It is a band of neural tissue on the cerebral cortex lying on precentral fissure. The body's movements are mapped out on this band giving rise to the spreading fashion that Jackson described during seizures (4).

Loss of GABA inhibition and hyperexcitability of the hippocampus

Experimental work has demonstrated that repeated or prolonged seizures (status epilepticus) cause hippocampal sclerosis, presumably through excessive activation of excitatory glutamate receptors, which results in excitotoxicity. Removal of sclerotic hippocampus leads to dramatic improvement or even a cure of the epileptic condition in humans, which suggests that the sclerotic hippocampus somehow causes the epilepsy. One could argue, however, that it is the other way around that these individuals have had hypoxic injury that may have caused the hippocampal sclerosis, which then caused the onset of seizures. In the absence of hypoxia though, it seems equally plausible that intense seizures can cause hippocampal sclerosis, which then can cause epilepsy (1).

Repeated and intense seizures cause a loss g-amino butyric acid (GABA)- mediated inhibition of dentate granule cells in vitro. Thus until recently the leading hypothesis was that death of GABAergic inhibitory internuerons resulted in attenuation of inhibition, which in turn lead to hyperexcitability of the remaining neurons of the hippocampus. However, detailed immunohistcohemical studies of sclerotic hippocampus isolated from experimental models and from humans have provided new potential mechanisms of hyperexcitability. In work that contradicted the prevailing idea at the time, Sloviter demonstrated in an experimental model that GABA neurons were actually more resistant to seizure induced neuronal death than were other hippocampal neurons. Further, the study of tissue from human epileptic surgical specimens confirmed the relative preservation of presumed GABAergic interneurons. In fact, another type of cells was readily destroyed in these specimens-- mossy cells. Mossy cell are located in the dentate hilus (a part of the hippocampus) and were found to be extremely sensitive to seizure induced neuronal death(1).

Mossy cells are the most common type of neuron in the hilus of dentate gyrus of hippocampus. They receive synaptic inputs both from dentate granule cells and from the entorhinal cortex. Mossy cells project both ipsilaterally (the same side) and contralaterally (to the opposite side) to the molecular layer of the dentate gyrus where they synapse on the granule cells. Functionally, mossy cells are more activating by perforant path stimulation at a low threshold than the dentate granule cells and are thought to be excitatory on the granule cells. Mossy cells are damaged following intense synaptic activation, probably through excitotoxic mechanisms of activation of N-methyl-D-aspartate (NMDA) subtype of glutamate receptors which results in excessive intracellular calcium (1).

These series of findings lead to the dormant basket cell hypothesis which suggests that the seizure induced death of excitatory neurons in the hilus (probably mossy cells) removes an excitatory projection to GABAergic basket cell, the inhibitory neurons in the dentate gyrus, resulting in disinhibition because basket cells lie dormant when they are not activated by mossy cells. Once initiated, one can imagine a vicious cycle in which a partial loss of this inhibition, combined with excitatory synaptic input, could lead to excessive firing of granule cells, more mossy cell death, further loss of GABAergic inhibition and so on, resulting in an epileptic condition long after the initial injury. In an experimental model of unilateral hippocampal sclerosis from focal electrical status epilepticus, the resulting hyperexcitability of hippocampal neurons was stopped by stimulating the unaffected contralateral hippocampus. One explanation is that dormant basket cells were awakened by preserved contralateral mossy cells projections crossing through the hippocampal commisure (1).

The relationship between GABA inhibition and seizure is further supported by the fact that many of the antiepileptic medications act on GABA receptors. For example, the new antiepileptic drug, tiagabine, inhibits GABA uptake (7). This sort of clinic observation suggests that GABA does play a role in epilepsy.

Genetic Epilepsy

Shoffner et. al. were the first to identify the genetic defect in a human epileptic syndrome. Consistent with maternal inheritance, a mutation of a mitochondrial gene encoding a mitochondrial tRNA coding for lysine was found to be responsible for a condition characterized by myoclonic epilepsy and by a myopathy with a distinctive histochemical abnormality referred to as ragged-red fibers. This disease is known as the myoclonic epilepsy and ragged-red fibers (MERRF) syndrome. It is associated with defects in mitochondrial oxidative phosphorylation. The mitochondrial abnormality in the neurons will have negative effects on aerobic respiration and will lead to neuronal dysfunction underlying the myoclonic seizures (1).

Linkage analyses have successfully identified the chromosomal localization of the mutant genes underlying three different genetic epilepsies: benign neonatal convulsions, progressive myoclonic epilepsy, and tuberous sclerosis. The success of positional clinging in detecting the responsible gene in diseases such as cystic fibrosis and Huntington's disease offers hope for similar success with these three types of epilepsy. Two classes of genes that may be candidates are glutamate receptor and potassium channel genes, both of which are involved in the regulation of neuronal excitability (1). Further inquiry on the genetics of epilepsy has suggested that partial and generalized epilepsies are genetically indistinct. Some genotypes raise the risk for both generalized and partial epilepsies (2).

Zinc and Epilepsy: A Puzzling Relationship

Ever since the discovery that zinc induces seizures in rats, it has resulted in the suggestion that the release of cellular zinc plays a major role in the generation and propagation of epileptic activity. However, as the evidence was gathered, many contradictions accumulated. It has been proposed that zinc may act to attenuate the GABA response and thereby elicit hyperexcitability of the neurons and thereby incur a seizure. Conversely, it has also been found that zinc may act as an inhibitory neurotransmitter decreasing the likelihood of a seizure. Some researchers have noted a post-seizure increase in the level of zinc in the brains of rats and mice while others research do not show an increase. These variations could be due to differing lag times between the seizure and the sacrifice. Zinc has also been implicated in the pathology of cell death in response to activation of glutamate receptors. All in all, there seems to be a connection between zinc and seizures, but there are too many contradictions to clarify the nature of the relationship (5).


At the beginning of this essay, epilepsy was described as is "a diverse collection of disorders" (1). After reviewing the many different models on the cause and/or mechanism of epilepsy, one fact becomes abundantly clear that what we call "epilepsy" is a collection of disorders that bringing about similar behaviors but that may be caused by totally different factors-zinc or genes or GABA.

It may also come to mind what is the importance of studying epilepsy. It came to my mind often in moments of frustration during this project too. To me, there are two main contributions to be made by the study of the pathogenesis of epilepsy. First, there are major therapeutic and diagnostic contributions. While there are antiepileptic drugs available that control most epileptic symptoms, understanding the underlying mechanism of epilepsy could revolutionize treatment and perhaps improve current drug therapies. Additionally, proper understanding of the mechanism could perfect a diagnosis down to the specific brain dysfunction. Second, there is a great deal to be learned about the mind itself by studying epilepsy. Temporal lobe epilepsy is focused in the hippocampus and amygdala. The function of these structures could be illuminated by the study of epilepsy. In fact, in an editorial for Brian and Cognition, it was said that epilepsy has "provided the greatest opportunity for the study of higher cortical functions" (6).

The last comment that I have on epilepsy is in regard to my trigger dispersion theory of epilepsy. I found through my research that my theory seems to fit best with the Jacksonian model. This make sense at some level since he and I both were making models based on observation alone-no immunohistochemical or genetic studies. My model could not describe the action of a generalized seizures; rather it describes the mechanism of partial seizures. The fact that partial seizure begin in the temporal lobe and spread from there is very similar to my theory as well. In sum, making my own anecdotal model made studying epilepsy more challenging. My own critical thinking on the subject helped me tremendously when it came time to sift through the current theories presented in this paper.


WWW Sources

1) Database for medical journals , Search for "epilepsy" in the "words in title or abstract" field. This article (Mechanisms of Epilepsy by Shin and McNamara) will be the first hit.

2) AMA Homepage: Archives of Neurology, by Ruth Ottman, PhD et. al.

3) The National Institutes of Health Homepage: Research in the News.Ruth Lew Guver

4) Houssay M.D., Bernando A. Human Physiology. McGraw-Hill Book Company: 1955.

5) The Ideal library , Search for Zinc Metabolism in the Brain by Cuajungco and Lees.

6) The Ideal library , Search for Guest Editorial in Brain and Cognition by Peter J. Snyder.

7) AMA Homepage: Archives of Neurology, by Basim M. Uthman et. al.



Continuing conversation
(to contribute your own observations/thoughts, post a comment below)

11/02/2005, from a Reader on the Web

Was recently diagnosed with Jacksonian Epilepsy. After research on the Web, I came to the conclusion that this malfunction of the brain can indeed be precipitated by Zinc, something my hospital doctors never considered. Conclusion, avoid ingestion of zinc. Take no more than the 15mgs that most good vitamin/mineral supplements contain. I am 62 years of age. My first episode two years ago was the result of untreated high blood pressure. After possible damage to the hippocampus from prolonged High BP, the recent episode was caused by zinc. Art Haberstich


Additional comments made prior to 2007
Well, after reading the article on GABA and it's influence on seizures in the brain, I am interested in knowing more about what causes GABA reduction in the brain. I have read Abram Hoffer's papers on treatment of schizophrenia with high doses of niacin and Vit C and often zinc. So, I am confused regarding the zinc issue. He and Dr. Pfeiffer found by hair analysis that many serial killers had high levels of copper and low levels of zinc in the brain. So, the only conclusion I can draw from this is to have nutrient and minerals analyzed via the best methods, one of them being hair analysis, before adding or subtracting nutrients. I am experiencing something called depersonalization and derealization disorder after 23 years on Xanax and also in a violent marriage. I had a nervous breakdown and then went off the Xanax cold-turkey as I thought it might have been the cause. In a second of time, my world went from emotional and connected to empty and dissociated and has remained the same since that time. This condition can be a symptom related to schizophrenia or bi-polar or be a condition all to itself. Daphne Simeon has written a book called "Feeling Unreal" that describes this syndrome. One med student hypothesizes that we are really experiencing temporal lobe malfunction and some may indeed have temporal lobe epilepsy. I have been having sleep disturbances for 23 years that they diagnosed as anxiety attacks or night terror but never tested me for seizures and that is what they feel like. That is why I was prescribed Xanax. When I take Xanax, they are gone. Also, when I take Xanax (GABA producing drug) then my tinnitus lessens significantly as well. I ,also, have found that I have chlamydia and herpes simplex that are viruses which act as neurotoxins that may have been the culprit all along. I also experience systemic yeast infection that I finally have somewhat under control by means of Argentyn Silver(atomic silver that is only prescribed by docs) I didn't realize how far these viruses and yeast infection had spread until I went off the Xanax which must have been masking the symptoms. What happens to the brain after years of severe depression, anxiety, trauma, environmental toxins and neurotoxic illnesses that cross the blood brain barrier? Does the brain just shut down? Do the adrenals just shut down? If there has been too much damage, can the brain be renewed in some way? Is there anyway to help GABA production and help heal the temporal lobe area without drugs? This condition, depersonalization clearly shows problems with temporal lobe, amygdala and parietal lobes. It is closely tied to anxiety attacks and post-traumatic trauma but can be related to drug usage or withdrawal. It is listed in the DSM under dissociative disorder and many doctor's do not know much about it. Would appreciate any input that anyone reading might have on these questions and thank you for reading ... Linda Stacip, 7 April 2006



I have written to you before concerning my work in dogs (and now more and more people) with epilepsy and the use of the glutamate-aspartate restricted diet (The GARD). The results have been ASTOUNDING, with every case that has been placed on this diet showing significant response and most having dramatic improvements. The basis for the diet is the elimination of all gluten, casein, soy, and corn...the four foods that induce villous atrophy of the duodenum. These foods are also HUGE sources of the non-essential, neurostimulating amino acids glutamate and aspartate (the parent amino acids in MSG and aspartamerespectively.

The reason for my contacting you again is my attempt to locate Carly Cenedella. I have enjoyed her articles and contributions to your site and really want to run the diet and phenomenal results I have seen over the past 6 years past her and get her response. Again, more and more people are writing to me and sharing their amazing testimonials on the diet. I do believe that it is THE epilepsy diet, showing MUCH better results than the ketogenic and modified Atkins diets. NONE of my now countless patients have had to undergo any ketosis.

Is it possible for you to contact her and ask her to contact me? I am in the process of writing journal articles and speaking to annual conferences of both veterinarians and MDs. In fact, I just spoke on this topic at the annual conference of the A4M ( Chicago this past weekend, an international meeting of over 4,000 MDs and PhDs.

My email is My Website is

Thanks for your help. Great site, BTW.:):):) ... John Symes 18 July 2006



The Perils of Vaccines: Epileptic Seizures and Schizophrenia


The following case study was submitted by a physician as a wake up call to young parents and enlightened doctors.


The perils of vaccines goes beyond just the cheap mercury preservative, Thimerosal, a known neurotoxin capable of destroying nerves and damaging brain tissue. The so called "gold" standard of testing, the "double blind" study is not even being used to validate vaccine "benefits". According to Dr. Sherri Tenpenny's research, the Center For Disease Control's (CDC) vaccine testing program provides multiple vaccines to one group of healthy children and only one vaccine to a second group of healthy children. And when adverse side effects are reported they are quickly dismissed as not having any relationship to the vaccine. The vaccine "researchers" do not even use a "placebo" in their "gold standard" testing. Most physicians are not even aware of this distorted testing technique and faulty reporting being used to snow the scientific community.


As if the unscientific testing and faulty reporting techniques are not bad enough, most physicians are not aware of the latent adverse residual effects of vaccines. Once injected into the body, the components of the vaccine travel through the blood stream and become trapped in organs and tissues of the body. Years later symptoms may surface. Very few healthcare practitioners will ever recognize the link. That was the case with J.B. an 8 year-old who was diagnosed by Children's Hospital, several top neurologists and psychiatrists as suffering from Epileptic Seizures and Schizophrenia. This child would go into altered states, not recognizing his parents and then calling them by different names. These altered states as well as the seizures would occur randomly and without obvious initiating events. Traditional medicine's solution was to prescribe anti-seizure and anti-hallucinogenic medications.


Using diagnostic testing based on quantum physics, J.B. was diagnosed as having Thimerosal in the right side of his brain and the residue of six vaccines in his liver. It is a well recognized fact among researchers that mercury in the brain is capable of causing epileptic seizures. Vaccine residues provide antigens or foreign substances, which can stimulate an allergic type reaction. The toxins released circulate throughout the blood stream eventually passing through the brain. The toxicity of these reactive substances, like taking multiple medications, will cause brain dysfunction similar to the elderly who experience hallucinations when taking too many drugs. Treatment involved natural chelating substances to pull the mercury out of the brain and homeopathic nosodes to neutralize the vaccine residues in the liver. In one month J.B. was back to normal and has not had a single episode of either a seizure or altered state since September 2006. The key to any successful medical treatment is to define the underlying cause and neutralize it with natural remedies. This concept has eluded allopathic or traditional medicine and is the primary reason why the "sick" care system is failing miserably ... Gerald H. Smith, 1 January 2007




Craig Davis's picture

wanting answers

I read most of everything here including the other comments, all to say my brain is still confused after reading what I did & after having seizures since 5 months old, which will be 58 years on Thanksgiving Day 2018. So WHY isn't there any simple pill in a form of a drug or supplement, that keeps stable all the GLUTAMATE & GABA levels normal in our human brain ?
Can it be as well that brain GLUCOSE in older people as well as teens & younger are unstable, as I had SO MANY Glucose Tolerance tests from 4 to 10 hour tests up to age 17 from age 9, where my glucose was ALWAYS a tell sign if I was having a good or bad 3, 4 or 6 month seizure activity, with petit mals, that I KNEW THEN foods triggered my seizures in those years & days BUT Who ever listens to kids & teens then or TODAY ? Now after my last G T T I had, & 45 years later I have GRAND MALS when I eat the wrong foods that can have MSG's & NITRATES/ITES in them, as that was they problem in the 60's & 70's to where today NO neurologists ever cares to talk about that to any of us living with seizures, young or old. So again I ask,,, Why a good supplement or a drug can not be made to control all 3 of GLUCOSE, GABA & GLUTAMATE,, which when I asked a neurologist I had at UVA in Virginia,, I was told I am living in a fantasy world, if I think that will ever happen in my lifetime before I die. I then said,,, What type of life do you think I am living now by taking AED's that you & other doctors put me on as I WAS TO BELIEVE they were going to STOP THE SEIZURES in my past 50 years or more of life ? Call that FANTASY too but you all make MONEY with those drugs we pop every day that are worthless to take. Right,, so I want something that STOPS the seizures, that you never care to give to me or any other neurologist. I am interested though in the XANAX that I read about. Is that too considered another AED ?

Serendip Visitor's picture

Seizures and Zinc

While I'm sure some of you will never read this, I can tell you with confidence, and from my own suffering that I do suffer seizures if I have too much zinc in my system. I used to take supplements to try to balance out my body and zinc was one of the supplements I took having taken them individually and I have spoken to my epileptologist about this and while this was not nor has been the key cause to my seizures it does cause me to have one some 12-24 hours after taking any as my seizures usually land me in the ER it's hard for me not to notice.

lily king's picture

ambien for control seizure

my daughter has seizure for 26 years, is on depakote, tegretol and kappre and still have tremors and big seizure, because recently, she even can not sleep at night, the Doc gives her 10mg of ambien before bed time, amazine, her seizure is gone and sleep well.
I have known, depakote works on GABA b receptor and tegretor works on GABA a receptor and ambien is working on GABA receptor in multiple sides.
Ambien is a drug, definitely worth to study deeply !

Serendip Visitor's picture

Denture adhesives and seizures

Hi, my husband has used a certain type of denture adhesive for over 21 years, and approximately 21/2 years ago he had his first seizure. The doctors are seeing two spots on his brain but are not saying they aare strokes. He also suffered from 2 compression fractures in his lower spinal cord, has no balane now, and has continued to have the seizures about about every 2 to 3 months. Just recently had 4 in 1 day. Can too much zinc in the body cause neurologic issues?

Keith Wilhelm's picture


I have partial epileptic seizures. For years I took phenyotin under the care of Dr. John Rheinhart practicing in Connecticut.
The counseling Dr. Rheinhart provided helped manage me. I am studying the etiology and mechanism of epilepsy to live a better life through knowledge of neurology, pharmacology, and medicine.

nikki's picture

i think learning about

i think learning about epilepsy is so allsome, but i have a project on epilpsy so i need more ifomation about this disorder the project is due in 1 week i all ready have some stuff about epilepsy but i need more infomation. I have the defination, some systyems, and how epilepsy begains, i jut need what caueses epilepsy and more things about this disorder. so if you can please can you send me more suff about epilepsy so
Thank You,

psoriasis homeopathy's picture

The use of Zinc in treatment

The use of Zinc in treatment of GABA is also mentioned in the ancient medicines like ayurveda but still it is not tested and proven in modern medicines.

Serendip Visitor's picture

Another way to look at the problem

Looking at the brain from and engineering perspective, the neurons are firing and not firing, and epilepsy is "too many of them firing", in some general sense. A normal, and stable pattern of firing would have to be a negative feedback loop. In other words, whenever the electrical activity is high, this would necessarily trigger systems that would reduce the level of activity. The system would not be stable otherwise. A simple example would be a thermostat controlling the temperature of a house, when the temperature of the house is high, it turns off the heater.
Is our brain network inherently stable? I have some doubts, seizures are not common, but they can be triggered by low glucose levels.
If our neural network is normal stable, what could cause it to become unstable? Take the example of the heater in the house, if the thermostat malfunctioned and turned the heat on when the house is hot, this would cause the house to overheat.
An obvious solution would be to eat GABA. It is readily available, why not just eat it as a dietary supplement?

Lee's picture

You can't EAT GABA as supplement

Hi there,

As a student researcher on Epilepsy/GABA, I just wanted to say that increasing GABA levels in the brain will technically relieve the symptoms but you need to know that GABA cannot cross the Blood Brain Barrier. Meaning, oral intake of GABA as a supplement will not do anything since it will not reach the brain. Currently the most promising drugs of epilepsy (or at least to increase the GABA levels in the brain) is GABA-AT (the enzyme catalyzes GABA into succinic semialdehyde in the brain) inhibitors. By inhibiting this GABA catabolizing enzyme, we can at least maintain the levels of GABA in the brain and prevent it from degrading.

I too, personally want to know the very fundamental reasons for low levels of GABA in the epilepsy patients.

Serendip Visitor's picture

eating more gaba

"An obvious solution would be to eat GABA."

If it a LACK of GABA inhibition, then higher GABA levels would exacerbate the problem.
Also, it far too simplistic to think eating GABA increases brain levels of GABA.

Spartacus's picture


Hi, just thought I will write about my personal experience.

My wife had been on anti-epilepsy medication (of all types) since childhood, and it seemed to be intractable. Not to mention, all medications had their crazy side effects. Some supposedly top doctors had tried to treat her, and they could only manage to suppress her seizures temporarily. The docs didn't seem to know more than prescribing the standard anti-epilepsy medications. Some suggested neuro-surgery treatments, which we both would simply not consider.

So, I tapered all her medications, and she trusted me enough to do that. I studied up and tried a huge number of alternative treatments - herbal, homeopathic, ayurvedic, all kinds of vitamins and supplements, etc. No processed food - only organic, etc. But nothing seemed to help much. I also kept a meticulous log of her reactions to everything (including every ingredient of every recipe), but couldn't make much sense of it - it seemed random and too complex, especially since I had to study up medical aspects of everything, and I didn't have a medical background to begin with. There seemed to be too many parameters to make sense of and to co-relate into a coherent hypothesis.
Meanwhile her seizures continued @ 1 per week or two.

But then I finally detected the pattern that her condition seemed to predictable worsen on intake of iron and iron-rich foods significantly. Also, drinking water stored in a copper vessel affected her adversely, too.

So, in conclusion (cu being a Zn competitor and iron lowering Zn absorption significantly), I constructed a hypothesis and tested it by putting her on zinc supplementation.
And hey presto, her petite mals stopped within (literally) 2-3 days of beginning the zinc, and she has had no grand mal seizure since then, and her mental state has improved remarkably. She is able to handle much larger amounts of stress without getting freaked out.
It just felt like magic, that a lifelong traumatizing affliction could be resolved just like that - with a snap of one's fingers.

So, absolutely, Zinc had worked like magic in my case. (Of course, other people's cases might be entirely different - one has to monitor things really meticulously, to derive the precise pattern).
But one thing I will say - docs don't know much beyond peddling the stuff that the pharma companies hypnotize them into peddling, and I don't know if many of them take any trouble to look beyond the standard dogma of the dominant paradigm.

criss's picture

Hi, my wife have some

Hi, my wife have some seizures in sleep, once a month or once at 6 monts.The doctor said that is not epilepsy.Can you tell me please what kind of zinc did you buy? I want to try this too.thanks

Joseph Brenner's picture

Another Look at Glutamate

Drs.Sidney Kurn and Sheryl Shook, in their 2008 book "Integrated Medicine For Neurologic Disorders" mention an irreversible metabolic conversion of Glutamic Acid to GABA, utilizing GAD and pyridoxal phosphate as co-factors, to convert the main excitotoxin into the main CNS inhibitor. They also point out research that implicates low levels of GABA in poor seizure control cases. Could this indicate a beneficial side to glutamate?

Serendip Visitor's picture

Glutamates and seizure

If the low levels of GABA imply a link between glutamates and seizure control, then why does there appear to be a correlation between untreated Celiac Sprue and seizures? And between MSG and seizures?

Concerned Mom's picture

epilepsy - hippocampus sclerosis

Thank you for the very interesting article.

At age 7, my son was diagnosed with nephrotic syndrome complicated by pneumococcal peritonitis, septic shock, acute renal failure requiring CVVH and hemodialysis, and severe hypertension and seizures (hypertensive encephalopathy).

At age 10, he was diagnosed with epilepsy (complex partial seizures). Prior to this diagnosis I now realize he was experiencing partial seizures that went undiagnosed for at least 9 months. The partial seizures were stomach pain that lasted for about 30 seconds and would occur multiple times per day.

Currently he is on his third seizure medication.

At age 12, he had a neuropsychological evaluation. Among the results of the evaluation were memory issues and problems with his fine motor skills. Also it was pointed out to me the possibility that the cause of his epilepsy is a result hippocampus sclerosis (resulting from the hypertensive encephalopathy at age 7).

This information was shared with his neurologist who recommended that he get an MRI with fine cuts focusing on the hippocampus.

After reading this article, I wonder why the neurologist didn't order the MRI long ago.

brenna's picture

re: what causes

re: what causes epilepsy?

I'm not sure if I really understand what was wrtten, but I have a 25 yr old son that was involved in a Motor Vehicle accident 2 yrs ago & has a severe brain injury...he is unable to walk, talk, & is fed via PEG because of his inabliltiy to swallow - After watching an episode of 60 Minutes re; the medication Ambien & it's ability to help another brain injured young man, we gave my son Ambien & he spoke for the first time in a year and a only last about an hour, but he also is able to swallow & eat and tries his best to stand & his spasticty lessons.....Just last week he was given Ativan in the Emergency Room to relax him after he pulled out his feeding tube & instead of relaxing him, he became animated & spoke & ate for over 8 hours...I really don't read this type of medical literature well, but from what I gather it appears that GABA has something to do with both of these medications..

My question since reading your article is, could my son, David, possibly benefit from some type of anti-seizure medication? i know most people w/brain injury take seizure medication, but since David has not shown to have seizures (that we have been able to see) he was never put on anti-seizure medication...I'm afraid to give him the Ativan and I give him Ambien every day, but it is so short acting...Do you have any thoughts on this???

David's mom, Brenna