Seizure Disorders


What should I know about Seizure Disorders or Epilepsy?

Epilepsy (also known as seizure disorder) is a neurological condition with symptoms which vary from a momentary lapse of attention to convulsions. What it is has been understood. What causes it is often not understood. Epilepsy was one of the first brain disorders to be described and its history goes back some 3000 years when it was first mentioned in Babylon. The word epilepsy is derived from the Greek word for "attack." It was once thought that people who had epilepsy were being visited by demons or gods. However in 400 B.C., the early physician Hippocrates suggested that epilepsy was a disorder of the brain.

A seizure disorder includes any condition in which there are repeated episodes of seizures of any type. Damage to brain cells can disrupt the normally smooth-running pattern of electrical activity in the brain by causing an electrical overload. This can create a seizure, which causes a sudden change in the individual's consciousness and/or change in motor activity. Epilepsy (idiopathic seizure disorder) is a term used when the seizure disorder has no identifiable cause such as brain disease. A seizure disorder affects about 0.5% of the population, and may affect people of any age. (1) The symptoms, frequency, intensity, and types of seizures vary greatly from person to person. Those whose condition is controlled by medication may not experience seizures at all.

In many cases, the cause of epilepsy is unknown. (2) It can occur as a result of an infection, head injury, brain tumor, hydro-cephalus, toxic reaction to drugs and alcohol, or other conditions which injure the brain and damage brain cells. (3) , (4) Genetic factors may contribute to the development of a seizure disorder, but are not a primary cause. (5) It may also be associated with other neurological conditions such as cerebral palsy. The cause of the seizure correlates to some extent with how old the person is when the first seizure occurs. In some people, seizures may be triggered by hormone changes such as pregnancy or menstruation. They may also be triggered by illness or by sensory stimuli such as lights, sounds, and touch. In many cases, no trigger is found for the seizures. Though no direct link to seizures has been confirmed, people who have seizures have been shown to have low blood levels of vitamin A, vitamin C and vitamin E. (6)

Seizures may occur in a generalized form (affecting all or most of the brain) or in a partial form. Epilepsy is typically generalized (except in some cases that develop in childhood and have a specific focus). Generalized seizures include variations of what are referred to as generalized tonic-clonic seizures and petit mal seizures. Partial seizures include focal seizures (during which the person remains alert but there are abnormal movements or sensations) and partial complex seizures (during which the abnormal movement or sensation is accompanied by changes in consciousness).


World Health Organization, 2001.

  • Up to 5% of the world's population may have a single seizure at some time in their lives.

  • 50 million people in the world have epilepsy.

National Institute of Neurological Disorders and Stroke, National Institute of Health, 1999.

    About 60 percent of people with epilepsy have partial seizures. 20 percent — about 600,000 people with epilepsy in the United States — have intractable seizures. 400,000 feel they get inadequate relief from available treatments. Approximately one in every 25 children will have at least one febrile seizure, and more than one-third of these children will have additional febrile seizures before they outgrow the tendency to have them. Febrile seizures usually occur in children between the ages of 6 months and 5 years and are particularly common in toddlers. Children rarely develop their first febrile seizure before the age of 6 months or after 3 years of age. The older a child is when the first febrile seizure occurs, the less likely that child is to have more. Between 95 and 98 percent of children who have experienced febrile seizures do not go on to develop epilepsy.

Signs and Symptoms

[span class=alert]The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.[/span]

Epilepsy is defined as seizures of any type that can occur multiple times over many years and have no known cause. In general the individual will also have the following symptoms: headache, mood changes, changes in energy levels, dizziness, confusion, fainting, and memory loss. An aura or sensation that indicates that a seizure may occur, happens in some but not every individual.   Petit mal seizures

  • Minimal or no movements such as "eye blinking"
  • Sudden loss of awareness or conscious activity
  • Recurs many times
  • Occurs most often during childhood
  • Can decrease learning
Grand mal seizures (Generalized tonic-clonic)
  • Violent muscle contractions
  • Can affect major portions of the body
  • Loss of consciousness or awareness
  • Breathing stops temporarily, then "sighing"
  • Loss of control of bladder
  • Biting of tongue and cheeks
Single focal seizures
  • Muscle contractions of a specific body part
  • Abnormal sensations
  • May have nausea, sweating, skin flushing, and dilated pupils
  • May have other symptoms
Partial complex seizures
  • Abnormal sensations
  • May have nausea, sweating, skin flushing, and dilated pupils
  • May have other symptoms
  • Emotions may be inappropriate for the situation
  • Changes in personality or alertness
  • May or may not lose consciousness
  • May experience strange smells and tastes
Status epilepticus
  • More than 30 minutes of continuous seizures or two or more seizures without recovery between the seizures
  • More common in the younger child with most children being under the age of 3
  • This type of seizure can be convulsive or non-convulsive

Treatment Options


Treatment of epilepsy is aimed at controlling seizures as well as treating their underlying cause if it is known. Drugs in a category called oral anticonvulsants prevent or minimize the number of future seizures. The way an individual responds to the medication is completely individual, and the medication used and dosage may have to be adjusted repeatedly.

Nutritional Suplementation

Vitamin D

The most commonly prescribed anti-seizure medications, including phenobarbital, phenytoin, and carbamazepine, inhibit the vitamin D metabolism. (7) , (8) In addition to depleting vitamin D levels, this also interferes with the body’s ability to absorb calcium. Interference with vitamin D and calcium metabolism can cause the development of skeletal problems. Although these individuals are likely to be deficient in calcium, calcium supplementation is not warranted. The correct therapeutic intervention is to provide adequate levels of supplemental vitamin D, which will enable normalization of calcium absorption.

Folic Acid

Folic acid metabolism is interfered with by all of the primary anticonvulsant medications. (9) This increases the risk of birth defects, cervical dysplasia, anemia, cardiovascular disease (from elevated homocysteine), depression, and breast and colorectal cancers. (10) , (11) , (12) , (13) Before adding folic acid as a supplement, however, the physician prescribing the treatment drug must be consulted due to some potential interactions.


Prolonged magnesium deficiency can result in neurologic symptoms, including seizure, coma, and death. Neurological disturbances, including hyperexcitability, convulsions, and psychiatric disturbances can occur in individuals with severe magnesium deficiency and these problems can be corrected with appropriate magnesium supplementation. (14) Magnesium deficiency is seldom a cause of epilepsy but in rare cases, magnesium supplementation has been life-saving in patients who were suffering from acute intractable seizures due to magnesium deficiency. (15)


Research results determined that blood, and possibly hair manganese levels, were substantially lower in individuals with epilepsy compared to controls. Even though some patients did not exhibit reduced tissue manganese levels, patients with a higher frequency of seizures had the lowest manganese levels, suggesting that lower tissue manganese levels might be associated with higher seizure activity.

Herbal Suplementation


Vinpoceptine has anticonvulsant action, possibly linked to its neuronal protective capacity and/or its modulation of several chemical transmitter systems. (16) , (17) In these respects vinpocetine resembles adenosine, thought to be a major endogenous anticonvulsant and cerebral protectant.


If the seizure disorder is related to sugar metabolism, then gymnema may be of use. The leaves of gymnema are thought to increase insulin secretion, and several studies report control of hyperglycemia in moderately diabetic laboratory animals. (18) , (19) Human studies have reported a significant reduction in blood glucose during therapy with gymnema. (20) , (21)


  1. Hauser WA, Herdorffer DC. Epilepsy: frequency, causes and consequences. New York: Demos Publications; 1990.
  2. View Abstract: Dichter MA, Ayala GF. Cellular mechanics of epilepsy: a status report. Science. 1987;237:157.
  3. View Abstract: Olson KR, Kearney TE, Dyer JE, et al. Seizures associated with poisoning and drug overdose. J Emerg Med. 1993;11(6):565.
  4. View Abstract: Garcia PA, Alldredge BK. Drug induced seizures. Neurol Clin. 1994;12(1):85.
  5. View Abstract: Ottman R, Annegers JF, Hauser WA, et al. Higher risk of seizures in offspring of mothers than fathers with epilepsy. Am J Hum Genet. 1988;43:257.
  6. View Abstract: Sudha K, Rao AV, Rao A. Oxidative stress and antioxidants in epilepsy. Clin Chim Acta. Jan2001;303(1-2):19-24.
  7. View Abstract: Feldkamp J, et al. Long-term anticonvulsant therapy leads to low bone mineral density--evidence for direct drug effects of phenytoin and carbamazepine on human osteoblast-like cells. Exp Clin Endocrinol Diabetes. 2000;108(1):37-43.
  8. View Abstract: Zerwekh JE, et al. Decreased serum 24,25-dihydroxyvitamin D concentration during long-term anticonvulsant therapy in adult epileptics. Ann Neurol. Aug1982;12(2):184-6.
  9. View Abstract: Apeland T, et al. Folate, homocysteine and methionine loading in patients on carbamazepine. Acta Neurol Scand. 2001 May;103(5):294-9.
  10. View Abstract: Butterworth CE Jr, et al. Folate deficiency and cervical dysplasia. JAMA. 1992 Jan 22-29;267(4):528-33.
  11. View Abstract: Parnetti L, et al. Role of homocysteine in age-related vascular and non-vascular diseases. Aging (Milano). 1997 Aug;9(4):241-57.
  12. View Abstract: Mattson MP, Kruman II, Duan W. Folic acid and homocysteine in age-related disease. Ageing Res Rev. 2002 Feb;1(1):95-111.
  13. View Abstract: de Lumley L, et al. [Megaloblastic anemia in children]. Arch Pediatr. 1994 Mar;1(3):281-8.
  14. Yasui M, et al. Magnesium-Related Neurological Disorders. Mineral and Metal Neurotoxicology. 1997;22:219-226.
  15. View Abstract: Nuytten D, et al. Magnesium deficiency as a cause of acute intractable seizures. J Neurol. Aug1991;238(5):262-4.
  16. View Abstract: Schmidt J. Comparative studies on the anticonvulsant effectiveness of nootropic drugs in kindled rats. Biomed Biochim Acta. 1990;49(5):413-9.
  17. View Abstract: Molnar P, et al. Vinpocetine is as potent as phenytoin to block voltage-gated Na+ channels in rat cortical neurons. Eur J Pharmacol. Feb1995;273(3):303-6.
  18. Srivastava Y, et al. Hypoglycemic and Life-prolonging Properties of Gymnema sylvestre Leaf Extract in Diabetic Rats. Isr J Med Sci. Jun1985;21(6):540-42.
  19. View Abstract: Okabayashi Y, et al. Effect of Gymnema sylvestre, R.Br. On Glucose Homeostasis in Rats. Diabetes Res Clin Pract. May1990;9(2):143-48.
  20. View Abstract: Baskaran K, et al. Antidiabetic Effect of a Leaf Extract from Gymnema Sylvestre in Non-insulin-dependent Diabetes Mellitus Patients. J Ethnopharmacol. Oct1990;30(3):295-300.
  21. View Abstract: Shanmugasundaram ER, et al. Use of Gymnema sylvestre Leaf Extract in the Control of Blood Glucose in Insulin-dependent Diabetes Mellitus. J Ethnopharmacol. Oct1990;30(3):281-94.