eMedicine Specialties > Neurology > Seizures and Epilepsy

Seizures and Epilepsy, Overview and Classification: Treatment & Medication

Author: Jose E Cavazos, MD, PhD, FAAN, Associate Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, University of Texas Health Science Center at San Antonio; Co-Director, South Texas Comprehensive Epilepsy Center; Director of the Epilepsy Center, Audie L Murphy Veterans Affairs Medical Center
Coauthor(s): Mark Spitz, MD, Professor, Department of Neurology, University of Colorado Health Sciences Center
Contributor Information and Disclosures

Updated: Nov 10, 2009

Treatment

Medical Care

The goal of treatment is to achieve a seizure-free status without adverse effects. This goal is accomplished in more than 60% of patients who require treatment with anticonvulsants. However, many people have adverse effects, and some have seizures that are refractory to medical therapy. Monotherapy is important because it decreases the likelihood of adverse effects and avoids drug interactions. In addition, monotherapy may be cheaper than polytherapy, as many of the anticonvulsants have hepatic enzyme–inducing properties that decrease the serum level of the concomitant drug, increasing the required dose of the concomitant drug.

People with seizures experience psychosocial adjustments after their diagnosis; therefore, social and/or vocational rehabilitation may be needed. Many physicians underestimate the consequences that epilepsy may have on patients. For instance, patients with epilepsy may live in fear of experiencing the next seizure, and they may be unable to drive or work at heights.

Special situations in which treatment is needed

  • The mainstay of therapy for people with recurrent unprovoked seizures is an anticonvulsant. If a patient has had more than 1 seizure, administration of an anticonvulsant is recommended. On the contrary, standard of care for a single, unprovoked seizure is avoidance of typical precipitants (eg, alcohol, sleep deprivation); no anticonvulsants are recommended unless the patient has risk factors for recurrence.
  • The risk of recurrence in the 2 years after a first unprovoked seizure is 15-70% depending on several factors, mainly an abnormal brain MRI, an abnormal sleep-deprived EEG, and a partial-onset seizure.
    • The abnormal brain MRI finding refers to a possible substrate for an epileptogenic zone; therefore, it most often suggests that the brain injury that led to epilepsy is in the cortical and limbic regions. Diffuse abnormalities, such as hydrocephalus, might increase the risk by injuring the cerebral cortex.
    • An abnormal sleep-deprived EEG can include any or several abnormalities: epileptiform discharges, focal slowing, diffuse background slowing, and intermittent diffuse intermixed slowing. Epileptiform abnormalities and focal slowing are associated with an increased risk of seizure recurrence compared with the other findings. Nevertheless, the risk of recurrence in a person with 1 generalized tonic-clonic seizure, a normal EEG, a normal brain MRI, and no evidence of focal onset is about 15%; this patient is not treated. If a patient has all risk factors, the risk is approximately 80%; this patient is treated.
  • The major unresolved question is how to treat patients with 1 abnormality with a risk of 30-50%. When the present authors have such a patient, they discuss the possibilities, including risk of seizure recurrence, risk of toxic effects from taking the anticonvulsant, and benefits of avoiding another seizure, with the patient. The authors also discuss seizure precautions, including not driving for a specific time. Treatment with anticonvulsants does not alter the natural history of seizure recurrence; it only masks the risk for the duration of treatment.
  • The First Seizure Trial Group randomly selected 397 patients with an unprovoked, generalized tonic-clonic first seizure to take a conventional anticonvulsant (ie, carbamazepine, phenobarbital, phenytoin, valproic acid) or no treatment.18 About 18% of treated patients had seizure recurrence in 1 year, compared with 39% of untreated patients. Therefore, patients must be told that anticonvulsants reduce the risk of their having another seizure but that anticonvulsants do not totally stop seizures from recurring.

Treatment with anticonvulsants

  • The mainstay of treatment is anticonvulsant medication.
  • The type of seizure and the specific epileptic syndrome play a role in the selection of anticonvulsants, probably because of the different pathophysiologic mechanisms.
  • Some anticonvulsants (eg, lamotrigine, topiramate, valproic acid, zonisamide) have multiple mechanisms of action, and some (eg, phenytoin, carbamazepine, ethosuximide) have only 1 known mechanism of action. Anticonvulsants can be divided into 8 large groups based on their mechanisms, as follows:
    1. Blockers of repetitive activation of sodium channel - Phenytoin, carbamazepine, oxcarbazepine, lamotrigine, topiramate
    2. Enhancer of slow inactivation of sodium channel - Lacosamide, rufinamide
    3. GABA-A receptor enhancers - Phenobarbital, benzodiazepines
    4. Glutamate modulators - Topiramate, lamotrigine, felbamate
    5. T-calcium channel blockers - Ethosuximide, valproate
    6. N- and L-calcium channel blockers - Lamotrigine, topiramate, zonisamide, valproate
    7. H-current modulators - Gabapentin, lamotrigine
    8. Blockers of unique binding sites - Gabapentin, levetiracetam
    9. Carbonic anhydrase inhibitors - Topiramate, zonisamide

Anticonvulsive treatments for specific types of seizures

  • Absence seizures: If only absence seizures are present, most neurologists treat them with ethosuximide. If absence seizures are present with other types (eg, generalized tonic-clonic seizures, myoclonic seizures), the choices are valproic acid, lamotrigine, or topiramate. Do not use carbamazepine, gabapentin or tiagabine because they might exacerbate absence seizures. Whether pregabalin, a medication related to gabapentin, might also exacerbate this type of seizure is uncertain.
  • Tonic or atonic seizures: Tonic or atonic seizures typically indicate clinically significant brain injury. The Lennox-Gastaut syndrome is 1 common example of tonic seizures and best treated with broad-spectrum drugs (eg, valproic acid, lamotrigine, topiramate) or felbamate as last resort. Clinical trials of levetiracetam and zonisamide are being conducted. Other modalities include the use of vagal nerve stimulation (VNS). Recently a new agent, rufinamide (Banzel), was approved as adjunctive therapy for seizures associated with Lennox-Gastaut syndrome.
  • Myoclonic seizures: This seizure has a bimodal distribution. Infants with myoclonic epilepsies usually have a poor prognosis; however, in late childhood and adolescence, the syndrome of JME is often the cause of myoclonic seizures. JME is typically a benign process that is treated easily, but it has a high recurrence rate of approximately 80-90% after discontinuation of anticonvulsants. The best medications for JME and myoclonic seizures are valproic acid, lamotrigine, and topiramate. Levetiracetam has been approved by the FDA for adjunctive therapy of JME; this is the first medication approved for this syndrome. Anecdotal evidence suggests that zonisamide might be helpful in JME.
  • Primary generalized tonic-clonic seizures: This seizure type responds to valproic acid, topiramate, or lamotrigine. Levetiracetam has gained recent FDA approval as adjunctive therapy.
    • The Generalized Seizures arm of the SANAD trial demonstrated that "Valproate is better tolerated than topiramate and more efficacious than lamotrigine, and should remain the drug of first choice for many patients with generalized and unclassified epilepsies. However, because of known potential adverse effects of valproate during pregnancy, the benefits for seizure control in women of childbearing years should be considered."19 Levetiracetam and zonisamide were not included in this trial, which only tested lamotrigine, topiramate and valproate.
  • Partial-onset seizures: Carbamazepine is considered first-line therapy. However, in special populations, lamotrigine, oxcarbazepine, and topiramate might be better choices. Adjunctive therapy with levetiracetam, tiagabine, gabapentin, or pregabalin might be a choice if the first or second monotherapy trial with first line treatments failed.
    • The Veterans Administration (VA) Cooperative Study I clearly demonstrated similar efficacies for carbamazepine, phenytoin, primidone, and phenobarbital. Carbamazepine and phenytoin were tolerated better by men than women.20
    • The VA Cooperative Study II showed that carbamazepine and valproic acid had similar efficacies. However, in subset analysis for complex partial seizures, carbamazepine might be a better choice than valproate.21
    • The VA Cooperative Study of the treatment of seizures in the elderly (patients aged 60 y or older) was a comparison of carbamazepine, lamotrigine, and gabapentin. Lamotrigine and gabapentin were better tolerated than carbamazepine and similarly effective. Gabapentin caused more adverse effects than lamotrigine. The results led to the recommendation of lamotrigine as first-line monotherapy in elderly patients.22
    • The partial seizures arm of the SANAD trial demonstrated that although carbamazepine is the standard drug treatment, lamotrigine is clinically better for time to treatment failure outcomes. This study determined lamotrigine a cost-effective alternative to carbamazepine for patients with partial-onset seizures. This trial included carbamazepine, gabapentin, lamotrigine, oxcarbazepine, and topiramate.23
    • All new medications have been tested as adjunctive therapy, and head-to-head comparisons between new drugs and carbamazepine have been conducted in Europe. In general, the new drugs have similar statistical efficacies but fewer adverse effects than carbamazepine. The American Academy of Neurology and the American Epilepsy Society assembled a task force that reviewed the literature and provided evidence-based recommendations for monotherapy, adjunctive therapy, treatment of primary generalized seizures, treatment in children, and treatment of subgroups of new-onset and refractory epilepsy.24,25 Of the new anticonvulsants, lamotrigine and topiramate appeared to have broad spectrum of action in many seizure types.
    • If carbamazepine fails to control the seizures, lamotrigine, topiramate, tiagabine, gabapentin, levetiracetam, oxcarbazepine, pregabalin and zonisamide are considered for second- or third-line therapy. Several new anticonvulsants, including lamotrigine, topiramate, and oxcarbazepine, are indicated as monotherapy.
    • Although the new anticonvulsants are considered second- or third-line therapy, they can be used as first-line therapy in some patients.
    • Discussing the adverse-effect profiles of anticonvulsants with patients is important, because the efficacies of anticonvulsants appear to be similar.
  • Future advancements will involve antiepileptic drugs that alter the natural history of epilepsy. Evidence in animal models of epilepsy suggests that at least 2 of the current anticonvulsants, topiramate and levetiracetam, have neuroprotective effects and that they might slow the natural history of epilepsy. However, the applicability of animal data to human patients is unknown.

Anticonvulsive treatments for different patient populations

  • The use of anticonvulsants is slightly different in several populations of patients, including neonates, children, elderly patients, pregnant women, and patients with hepatic or renal insufficiency.
  • Neonates and children: Children and neonates tend to require similar loading doses per kilogram of body weight, but they tend to metabolize the drugs faster than adults. They also have rapid increases in the total volume of distribution.
  • Elderly patients: Elderly patients present the opposite problem to that of neonates and children. Slowed hepatic metabolism, decreased renal clearance, and decreased volumes of distribution are normal features of the aging process. These features mean a need for lowered initial and maintenance doses in elderly adults.
  • Women's issues: Enzyme-inducing anticonvulsants, such as carbamazepine, phenytoin, phenobarbital, primidone, felbamate, lamotrigine, topiramate, and oxcarbazepine, decrease the efficacy of birth control pills. Some anticonvulsants cause this drug interaction in a dose-dependent manner, with a negligible effect at low doses. Some obstetricians use a high-dose estrogen-progesterone pill. An alternative and possibly preferred approach is to use a second method of contraception.
    • Woman of childbearing age should take folic acid at least 1 mg/d to decrease the rate of neural-tube malformations in the fetus.
    • Evidence strongly suggests that, during pregnancy, women should take the medication that best controls their epilepsy. Switching medications during pregnancy is not recommended because of the risk of losing seizure control.
    • Women should be treated with only 1 anticonvulsant rather than polytherapy. Data from Japan show an exponential risk of birth defects as anticonvulsants are added in polytherapy.
    • Drug serum levels should be obtained frequently because of the many physiologic changes that take place during pregnancy, including changes in volume of distribution, protein binding, and hepatic metabolism and erratic absorption. In particular, decreased serum concentration of lamotrigine in the third trimester is well documented.
    • The performance of amniocentesis is a personal decision between the woman and her obstetrician. The most important point is to have a clear idea about how the information obtained will be useful for clinical decision making.
    • New guidelines for the management of AEDs during pregnancy were issued by the American Academy of Neurology and American Epilepsy Society in 2009.26,27,28
  • Hepatic and renal insufficiency: Considerable data are available on the use of phenytoin in both conditions. However, phenytoin is not a preferred medication because of its nonlinear kinetics, hepatic autoinduction, numerous drug interactions, and high degree of protein binding. Among all anticonvulsants, phenytoin, valproic acid, and felbamate have been associated with acute hepatic injury. Gabapentin and levetiracetam are excreted mostly by means of renal clearance. Their doses could be adjusted for renal insufficiency. They are useful in patients with hepatic failure, especially when a drug-induced etiology is suspected. Lamotrigine, which is metabolized by means of glucuronidation, a phase II reaction, is also used in some patients with hepatic insufficiency.

Nonpharmacologic treatments

  • Diet: The ketogenic diet has a role in children with severe epilepsy. One major problem is that, despite television programs and a movie supporting its use, <10% of patients continue the diet after a year. Furthermore, any small carbohydrate intake (eg, lollypop, piece of candy) resets ketone metabolism for 2 weeks, eliminating antiseizure efficacy. The diet, which relies heavily on Crisco (shortening product), is difficult to maintain. The diet is unquestionably effective in some refractory cases, but the present authors do not consider this treatment in teenagers or adults unless all of their intake is being delivered by means of a gastric tube.
  • VNS: The VNS is a palliative device approved to treat medically refractory partial-onset epilepsy in adults. Some studies demonstrate its efficacy in partial-onset seizures and in a small number of patients with primary generalized epilepsy. Randomized studies showed modest efficacy at 3 months, but postmarketing experience shows delayed improvement in another group of patients. According to the manufacturer's registry, efficacy of the device at 18 months is 40-50%, where efficacy is defined as a reduction in seizures of 50% or more. Many patients report improvement in seizure intensity and general mood. However, seizure-free rates for pharmacologically intractable partial-onset epilepsy are <10%.

Discontinuation of anticonvulsants

  • After a person has been seizure free for typically 2-5 years, physicians consider discontinuing the medication. Many patients outgrow many epileptic syndromes of childhood and need not take anticonvulsants. On the contrary, the recurrence rate during adulthood for patients with JME is about 80-90% in 2 years despite many years of being seizure free with low doses of appropriate anticonvulsants. The relapse rate for adults is about 40-50%; for children, it is about 25%. This difference is probably due to the different epileptic syndromes that are prevalent in the 2 populations.
  • Many neurologists use the risk factors for new-onset seizures to assess patients for discontinuation of anticonvulsants. A normal sleep-deprived EEG and normal brain MRI lower the risk of relapse after discontinuation, whereas epileptiform or focal abnormalities on a sleep-deprived EEG and/or focal cortical abnormalities on a brain MRI significantly increase the risk.
  • Other factors associated with an increased risk of seizure recurrence after discontinuation include the following:
    • Abnormal EEG (worse if epileptiform discharges or focal abnormalities are present)
    • Abnormal brain MRI (especially injury in cortical and limbic regions)
    • Several seizure types (worse if tonic or atonic seizures are present)
    • High number and frequency of seizures
    • Long duration of epilepsy before the seizures are controlled
    • Short duration of seizure freedom
  • About 75% of relapses after discontinuation occur in the first year, and at least 50% of patients who have another seizure do so in the first 3 months. Therefore, advise the patients to observe strict seizure precautions (including not driving) during tapering and for at least 3 months after discontinuation, depending on state laws. Driving is an impediment in some patients, who may opt to continue therapy.
  • The present authors recommend that all anticonvulsants, except primidone, phenobarbital, and benzodiazepines, be gradually discontinued over 6-10 weeks, if they were used for a long period. Discontinue primidone, phenobarbital, and benzodiazepines over 10-16 weeks.

Surgical Care

  • The 2 major kinds of brain surgery for epilepsy are palliative and potentially curative.
    • A few years ago, the most common palliative surgery was anterior callosotomy. This surgery has been indicated for patients with intractable atonic seizures, who often have facial and neck injuries due to a fall. This surgery is still performed but rarely. The use of a VNS in such patients has reduced the need for anterior callosotomy.
    • Several curative surgeries are possible, including lobectomy and lesionectomy.
      • In general, the epileptogenic zone must be mapped by using video-EEG monitoring with intracranial electrodes unless the patient clearly has a unilateral temporal-lobe onset.
      • Outcomes of temporal-lobe surgeries are better than those for surgeries in other areas. If a patient has unilateral temporal-lobe seizures (as observed on video-EEG) and unilateral hippocampal sclerosis (as observed on brain MRI), the likelihood of a class I outcome (no seizures or only auras) at 2 years is 85%.
      • If another anticonvulsant is attempted in the same patient with medically refractory epilepsy, the likelihood of a class I outcome is <5% at 2 years. A patient with medically refractory epilepsy is one in whom 3 anticonvulsants with adequate serum concentrations fail because of lack of efficacy and not because of adverse effects. After 3 anticonvulsants fail, patients with partial-onset seizures should be referred to an epileptologist.
  • For further details concerning surgical treatment of epilepsy please refer to the articles Identification of Potential Epilepsy Surgery Candidates, Outcome of Epilepsy Surgery, and Presurgical Evaluation of Medically Refractory Epilepsy.

Consultations

  • The first level of referral is for diagnosis and treatment.
    • Consult a neurologist if recurrent spells have not been diagnosed or if they have not responded to conventional therapy with a first or second anticonvulsant.
    • Establishing the correct diagnosis is the first step in providing adequate treatment.
  • The second level of referral is to an epileptologist: Patients in whom at least 2, and preferably 3, anticonvulsants at adequate serum concentrations have failed should be referred to an epileptologist to consider all available therapies, including pharmacologic, dietary, and surgical treatments.

Diet

The ketogenic diet is an effective tool to improve seizure control in very select cases. It is very difficult to follow as it requires achieving a ketotic state. Fewer than 1 in 20 patients who started this diet will be following it a year later.

Anecdotal data is published about improvement of seizure frequency following the Atkins diet and taking fewer than 10 g of carbohydrates, but the data is only preliminary.29

Activity

The major problem for patients with seizures is the unpredictability of the next seizure. Five types of seizure precautions should be discussed with patients who have seizures, as listed below. These lifestyle precautions are clearly more applicable to some patients than others. Safety must be balanced with the risk for seizures. A patient with many poorly controlled, diurnal seizures might exercise more caution than a patient who has only nocturnal seizures.

  • Driving motorized vehicles: Recommendations vary depending on state laws and on whether the patient has seizures that occur exclusively during sleep. Consult current state and federal laws and regulations. For example, to resume commercial driving across state lines, a patient must have a 5-year seizure-free period. The recommendation for driving cars and trucks extends to the operation of other motorized vehicles, such as boats, motorcycles, and others. Aircraft pilots are typically no longer permitted to fly.
  • Water precautions: Common sense dictates that patients should not swim alone, and patients with seizures should be particularly aware being in the presence of an adult lifeguard who can pull them out of the water if needed. Wearing a life jacket in a boat is important. Activities as simple as taking a bath might be risky because a patient can drown with as little as an inch of water during the flaccid postictal phase. Patients who might have a seizure, eg, while waiting for the water to warm up, may have hot-water burns.
  • Heights: Patients with seizures might experience one, eg, while trying to fix a roof or during another activity at considerable height from floor.
  • Fire: Burns from injuries related to cooking are not uncommon.
  • Power tools: Caution with the use of power tools is required. In particular, supervision during their use is needed, and the use of safety devices, such as automatic shutoff switches, is recommended.

Medication

The anticonvulsant of choice depends on an accurate diagnosis of the epileptic syndrome. Please see the Medical Care section and refer to medications in the appropriate articles listed in the Introduction for specific types of epileptic seizures or syndromes. Additionally, a summary of antiepileptic mediations is provided in the eMedicine topic, Antiepileptic Drugs: An Overview.

More on Seizures and Epilepsy, Overview and Classification

Overview: Seizures and Epilepsy, Overview and Classification
Differential Diagnoses & Workup: Seizures and Epilepsy, Overview and Classification
Treatment & Medication: Seizures and Epilepsy, Overview and Classification
Follow-up: Seizures and Epilepsy, Overview and Classification
References

References

  1. Goodkin HP. The founding of the American Epilepsy Society: 1936-1971. Epilepsia. Jan 2007;48(1):15-22. [Medline].

  2. Luders H, Acharya J, Baumgartner C, et al. Semiological seizure classification. Epilepsia. Sep 1998;39(9):1006-13. [Medline].

  3. Loddenkemper T, Kellinghaus C, Wyllie E, Najm IM, Gupta A, Rosenow F. A proposal for a five-dimensional patient-oriented epilepsy classification. Epileptic Disord. Dec 2005;7(4):308-16. [Medline].

  4. Engel J Jr. Report of the ILAE classification core group. Epilepsia. Sep 2006;47(9):1558-68. [Medline].

  5. Wolf P. Basic principles of the ILAE syndrome classification. Epilepsy Res. Aug 2006;70 Suppl 1:S20-6. [Medline].

  6. Engel J Jr. A proposed diagnostic scheme for people with epileptic seizures and with epilepsy: report of the ILAE Task Force on Classification and Terminology. Epilepsia. Jun 2001;42(6):796-803. [Medline].

  7. Wolf P. Of cabbages and kings: some considerations on classifications, diagnostic schemes, semiology, and concepts. Epilepsia. Jan 2003;44(1):1-4; discussion 4-13. [Medline].

  8. Fisher RS, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, et al. Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia. Apr 2005;46(4):470-2. [Medline].

  9. Beghi E. The concept of the epilepsy syndrome: how useful is it in clinical practice?. Epilepsia. May 2009;50 Suppl 5:4-10. [Medline].

  10. Rho JM, Sankar R, Cavazos JE. Epilepsy: Scientific Foundations of Clinical Practice. New York, NY: Marcel Dekker; 2004.

  11. Houser CR, Esclapez M. Vulnerability and plasticity of the GABA system in the pilocarpine model of spontaneous recurrent seizures. Epilepsy Res. Dec 1996;26(1):207-18. [Medline].

  12. Sloviter RS. Status epilepticus-induced neuronal injury and network reorganization. Epilepsia. 1999;40(suppl 1):S34-9; discussion S40-1. [Medline].

  13. Scharfman HE, Schwartzkroin PA. Protection of dentate hilar cells from prolonged stimulation by intracellular calcium chelation. Science. Oct 13 1989;246(4927):257-60. [Medline].

  14. Cavazos JE, Das I, Sutula TP. Neuronal loss induced in limbic pathways by kindling: evidence for induction of hippocampal sclerosis by repeated brief seizures. J Neurosci. May 1994;14(5 Pt 2):3106-21. [Medline].

  15. Sutula T, Cascino G, Cavazos J, et al. Mossy fiber synaptic reorganization in the epileptic human temporal lobe. Ann Neurol. Sep 1989;26(3):321-30. [Medline].

  16. McCormick DA. Cellular mechanisms underlying cholinergic and noradrenergic modulation of neuronal firing mode in the cat and guinea pig dorsal lateral geniculate nucleus. J Neurosci. Jan 1992;12(1):278-89. [Medline].

  17. Hosford DA, Clark S, Cao Z, et al. The role of GABAB receptor activation in absence seizures of lethargic (lh/lh) mice. Science. Jul 17 1992;257(5068):398-401. [Medline].

  18. FIRST Group. Randomized clinical trial on the efficacy of antiepileptic drugs in reducing the risk of relapse after a first unprovoked tonic-clonic seizure. First Seizure Trial Group (FIRST Group). Neurology. Mar 1993;43(3 Pt 1):478-83. [Medline].

  19. [Best Evidence] Marson AG, Al-Kharusi AM, Alwaidh M, Appleton R, Baker GA, Chadwick DW. The SANAD study of effectiveness of valproate, lamotrigine, or topiramate for generalised and unclassifiable epilepsy: an unblinded randomised controlled trial. Lancet. Mar 24 2007;369(9566):1016-26. [Medline].

  20. Mattson RH, Cramer JA, Collins JF, et al. Comparison of carbamazepine, phenobarbital, phenytoin, and primidone in partial and secondarily generalized tonic-clonic seizures. N Engl J Med. Jul 18 1985;313(3):145-51. [Medline].

  21. Mattson RH, Cramer JA, Collins JF. A comparison of valproate with carbamazepine for the treatment of complex partial seizures and secondarily generalized tonic-clonic seizures in adults. The Department of Veterans Affairs Epilepsy Cooperative Study No. 264 Group. N Engl J Med. Sep 10 1992;327(11):765-71. [Medline].

  22. [Best Evidence] Rowan AJ, Ramsay RE, Collins JF, et al. New onset geriatric epilepsy: a randomized study of gabapentin, lamotrigine, and carbamazepine. Neurology. Jun 14 2005;64(11):1868-73. [Medline].

  23. [Best Evidence] Marson AG, Al-Kharusi AM, Alwaidh M, Appleton R, Baker GA, Chadwick DW. The SANAD study of effectiveness of carbamazepine, gabapentin, lamotrigine, oxcarbazepine, or topiramate for treatment of partial epilepsy: an unblinded randomised controlled trial. Lancet. Mar 24 2007;369(9566):1000-15. [Medline].

  24. French JA, Kanner AM, Bautista J, et al. Efficacy and tolerability of the new antiepileptic drugs I: treatment of new onset epilepsy: report of the Therapeutics and Technology Assessment Subcommittee and Quality Standards Subcommittee of the AAN and the AES. Neurology. Apr 27 2004;62(8):1252-60. [Medline].

  25. French JA, Kanner AM, Bautista J, et al. Efficacy and tolerability of the new antiepileptic drugs, II: treatment of refractory epilepsy. Report of the Therapeutics and Technology Assessment Subcommittee and Quality Standards Subcommittee of the AAAN and the AES. Neurology. Apr 27 2004;62(8):1261-73. [Medline].

  26. [Guideline] Harden CL, Hopp J, Ting TY, Pennell PB, French JA, Allen Hauser W, et al. Management issues for women with epilepsy-Focus on pregnancy (an evidence-based review): I. Obstetrical complications and change in seizure frequency: Report of the Quality Standards Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Epilepsia. May 2009;50(5):1229-36. [Medline].

  27. [Guideline] Harden CL, Meador KJ, Pennell PB, Hauser WA, Gronseth GS, French JA, et al. Management issues for women with epilepsy-Focus on pregnancy (an evidence-based review): II. Teratogenesis and perinatal outcomes: Report of the Quality Standards Subcommittee and Therapeutics and Technology Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Epilepsia. May 2009;50(5):1237-46. [Medline].

  28. [Guideline] Harden CL, Pennell PB, Koppel BS, Hovinga CA, Gidal B, Meador KJ, et al. Management issues for women with epilepsy--focus on pregnancy (an evidence-based review): III. Vitamin K, folic acid, blood levels, and breast-feeding: Report of the Quality Standards Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and the American Epilepsy Society. Epilepsia. May 2009;50(5):1247-55. [Medline].

  29. Kossoff EH, Turner Z, Bluml RM, Pyzik PL, Vining EP. A randomized, crossover comparison of daily carbohydrate limits using the modified Atkins diet. Epilepsy Behav. May 2007;10(3):432-6. [Medline].

  30. Benbadis SR, Luders HO. Epileptic syndromes: an underutilized concept. Epilepsia. Nov 1996;37(11):1029-34. [Medline].

  31. Brodie MJ, Dichter MA. Antiepileptic drugs. N Engl J Med. Jan 18 1996;334(3):168-75. [Medline].

  32. Dichter MA, Brodie MJ. New antiepileptic drugs. N Engl J Med. Jun 13 1996;334(24):1583-90. [Medline].

  33. Engel J Jr. Classifications of the International League Against Epilepsy: time for reappraisal. Epilepsia. Sep 1998;39(9):1014-7. [Medline].

  34. Engel J Jr. International classification: implications for neocortical epilepsies. Adv Neurol. 2000;84:119-24. [Medline].

  35. Engel J Jr. Surgery for seizures. N Engl J Med. Mar 7 1996;334(10):647-52. [Medline].

  36. Goldensohn ES, Porter RJ, Schwartzkroin PA. The American Epilepsy Society: an historic perspective on 50 years of advances in research. Epilepsia. Jan 1997;38(1):124-50. [Medline].

  37. Hauser WA, Hesdorffer D. Epilepsy: Frequency, Causes, and Consequences. New York, NY: Demos Medical; 1990.

  38. Hosford DA, Wang Y. Utility of the lethargic (lh/lh) mouse model of absence seizures in predicting the effects of lamotrigine, vigabatrin, tiagabine, gabapentin, and topiramate against human absence seizures. Epilepsia. Apr 1997;38(4):408-14. [Medline].

  39. McNamara JO. Cellular and molecular basis of epilepsy. J Neurosci. Jun 1994;14(6):3413-25. [Medline].

  40. Patsalos PN, Perucca E. Clinically important drug interactions in epilepsy: interactions between antiepileptic drugs and other drugs. Lancet Neurol. Aug 2003;2(8):473-81. [Medline].

  41. Sanchez-Vives MV, McCormick DA. Cellular and network mechanisms of rhythmic recurrent activity in neocortex. Nat Neurosci. Oct 2000;3(10):1027-34. [Medline].

  42. Scheuer ML, Pedley TA. The evaluation and treatment of seizures. N Engl J Med. Nov 22 1990;323(21):1468-74. [Medline].

  43. Sloviter RS, Pedley TA. Subtle hippocampal malformation: importance in febrile seizures and development of epilepsy. Neurology. Apr 1998;50(4):846-9. [Medline].

  44. Sutula T, He XX, Cavazos J, Scott G. Synaptic reorganization in the hippocampus induced by abnormal functional activity. Science. Mar 4 1988;239(4844):1147-50. [Medline].

Further Reading

Keywords

epilepsy treatment, guidelines, seizure treatment, convulsions, epileptic seizures, classification of seizures, classification of epilepsy, partial-onset seizures, generalized-onset seizures, unclassified seizures, epileptic syndromes

Contributor Information and Disclosures

Author

Jose E Cavazos, MD, PhD, FAAN, Associate Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, University of Texas Health Science Center at San Antonio; Co-Director, South Texas Comprehensive Epilepsy Center; Director of the Epilepsy Center, Audie L Murphy Veterans Affairs Medical Center
Jose E Cavazos, MD, PhD, FAAN is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, American Epilepsy Society, and Society for Neuroscience
Disclosure: Nothing to disclose.

Coauthor(s)

Mark Spitz, MD, Professor, Department of Neurology, University of Colorado Health Sciences Center
Mark Spitz, MD is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society
Disclosure: pfizer Honoraria Speaking and teaching; ortho-mcneil Honoraria Review panel membership

Medical Editor

Ramon Diaz-Arrastia, MD, PhD, Assistant Professor, Department of Neurology, Comprehensive Epilepsy Center, University of Texas Southwestern
Ramon Diaz-Arrastia, MD, PhD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, New York Academy of Sciences, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

 
 
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