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Epileptic and Epileptiform Encephalopathies Medication

  • Author: Dean Patrick Sarco, MD; Chief Editor: Amy Kao, MD  more...
 
Updated: Dec 15, 2015
 

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and to prevent complications. The agents used in the treatment of epilepsy include anticonvulsants and adrenocorticotropic hormones.

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Adrenocorticotropic hormones

Class Summary

These agents stimulate the adrenal cortex to release of corticosteroids.

Corticotropin (ACTH, Acthar)

 

Efficacy in epileptic encephalopathies is variable. However, ACTH is associated with serious, potentially life-threatening side effects. ACTH gel preparation is used in epilepsy and is the only anticonvulsant medication that must be administered by IM injection.

Prednisone (Deltasone, Meticorten, Orasone)

 

Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing polymorphonuclear neutrophil (PMN) activity.

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Anticonvulsant agents

Class Summary

These agents prevent seizure recurrence and terminate clinical and electrical seizure activity. If absence seizures are present, ethosuximide is the appropriate medication. This may be the case for patients with chronic absence epilepsy. These agents may be used in conjunction with an anticonvulsive AED, such as phenytoin (Dilantin), for patients at risk of tonic-clonic seizures in whom valproic acid is contraindicated.

Vigabatrin (Sabril)

 

Vigabatrin inhibits gamma-aminobutyric acid transaminase (GABA-T), increasing the levels of the inhibitory compound GABA within the brain.

Carbamazepine (Tegretol)

 

Carbamazepine appears to act by reducing polysynaptic responses and blocking posttetanic potentiation. Its major mechanism of action is to reduce sustained high-frequency repetitive neural firing.

Diazepam (Valium)

 

A long-acting benzodiazepine, diazepam has anxiolytic and anticonvulsant properties. Diazepam is effective for multiple seizure types, but is usually used for control of intermittent episodes of increased seizure activity in epilepsy patients on stable anticonvulsant regimens.

Diazepam's mechanism of action is based on inhibition of neuronal excitation through binding to gamma-aminobutyric acid (GABA) and more specifically to GABA-A receptors.

This agent is available in oral solution (5 mg/5 mL or 5 mg/mL), tablets (Valium) 2 mg, 5 mg, 10 mg, rectal gel (Diastat or Diastat AcuDial delivery system and injection), and solution (5 mg/mL).

Valproic acid (Depakote, Depakene, Depacon)

 

Valproic acid is chemically unrelated to other drugs used to treat seizure disorders.

Although its mechanism of action is not established, the activity of valproic acid may be related to increased brain levels of GABA or enhanced GABA action. This agent may also potentiate postsynaptic GABA responses, affect potassium channels, or have direct membrane-stabilizing effect.

For conversion to monotherapy, concomitant AED dosage ordinarily can be reduced by approximately 25% every 2 wk. Reduction may be started at initiation of therapy or delayed by 1-2 wk if concern that seizures are likely to occur with reduction. Monitor patients closely during this period for increased seizure frequency.

As adjunctive therapy, valproic acid may be added to the patient's regimen at a dosage of 10-15 mg/kg/d. The dosage may be increased by 5-10 mg/kg/wk to achieve optimal clinical response. Ordinarily, optimal clinical response is achieved at daily doses of less than 60 mg/kg/d.

Ethosuximide (Zarontin)

 

A succinimide AED, ethosuximide is effective only against absence seizures. It has no effect on generalized tonic-clonic, myoclonic, atonic, or partial seizures.

The mechanism of action of ethosuximide is based on reducing current in T-type calcium channels found on thalamic neurons. The spike-and-wave pattern during petit mal seizures is thought to be initiated in thalamocortical relays by activation of these channels.

Ethosuximide is available in large 250-mg capsules, which may be difficult for some children to swallow, and as syrup (250 mg/5 mL).

Zonisamide (Zonegran)

 

Zonisamide may stabilize neuronal membranes and suppress neuronal hypersynchronization through action at sodium and calcium channels. It does not affect GABA activity.

Lamotrigine (Lamictal, Lamictal ODT, Lamictal XR)

 

Lamotrigine is a thiazine derivative that inhibits the release of glutamate (an excitatory amino acid) and inhibits voltage-sensitive sodium channels

Levetiracetam (Keppra, Keppra XR)

 

Levetiracetam has a mechanism of action that may involve inhibition of voltage-dependent, N-type calcium channels; facilitation of GABA-ergic inhibitory transmission through displacement of negative modulators; and reduction of the delayed rectifier potassium current.

Felbamate (Felbatol)

 

Felbamate is an oral antiepileptic agent with weak inhibitory effects on GABA-receptor binding and benzodiazepine receptor binding. It has little activity at the MK-801 receptor-binding site of the NMDA receptor-ionophore complex. However, felbamate is an antagonist at the strychnine-insensitive glycine recognition site of the NMDA receptor-ionophore complex.

Tiagabine (Gabitril)

 

The mechanism of action of tiagabine in antiseizure effects is unknown. It is believed to be related to its ability to enhance the activity of GABA, the major inhibitory neurotransmitter in the CNS.

Rufinamide (Banzel)

 

Rufinamide prolongs the inactive state of the sodium channels, thereby limiting repetitive firing of sodium-dependent action potentials, mediating anticonvulsant effects.

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Contributor Information and Disclosures
Author

Dean Patrick Sarco, MD Instructor, Department of Neurology, Harvard Medical School; Assistant Physician, Department of Neurology, Division of Epilepsy and Clinical Neurophysiology, Children's Hospital Boston

Dean Patrick Sarco, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Child Neurology Society

Disclosure: Nothing to disclose.

Coauthor(s)

Masanori Takeoka, MD Assistant Professor, Department of Neurology, Harvard Medical School; Staff Physician, Department of Neurology, Division of Epilepsy and Clinical Neurophysiology, Boston Children's Hospital

Masanori Takeoka, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Medical Association, Child Neurology Society, Massachusetts Medical Society

Disclosure: Nothing to disclose.

Chief Editor

Amy Kao, MD Attending Neurologist, Children's National Medical Center

Amy Kao, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, Child Neurology Society

Disclosure: Have stock from Cellectar Biosciences; have stock from Varian medical systems; have stock from Express Scripts.

Acknowledgements

Robert J Baumann, MD Professor of Neurology and Pediatrics, Department of Neurology, University of Kentucky College of Medicine

Robert J Baumann, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, and Child Neurology Society

Disclosure: Nothing to disclose.

Jose E Cavazos, MD, PhD, FAAN Associate Professor with Tenure, Departments of Neurology, Pharmacology, and Physiology, Program Director, Clinical Neurophysiology Fellowship, University of Texas School of Medicine at San Antonio; Co-Director, South Texas Comprehensive Epilepsy Center, University Hospital System; Director of the Epilepsy and Neurodiagnostic Centers, 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, American Neurological Association, and Society for Neuroscience

Disclosure: GXC Global, Inc. Intellectual property rights Medical Director - company is to develop a seizure detecting device.

Stavros M Hadjiloizou, MD Instructor, Department of Neurology, Division of Epilepsy and Clinical Neurophysiology, Children's Hospital, Harvard University Medical School

Stavros Michael Hadjiloizou is a member of the following medical societies: American Academy of Neurology, American Academy of Pediatrics, American Epilepsy Society, American Medical Association, Child Neurology Society, and Massachusetts Medical Society

Disclosure: Nothing to disclose.

James J Riviello Jr, MD George Peterkin Endowed Chair in Pediatrics, Professor of Pediatrics, Section of Neurology and Developmental Neuroscience, Professor of Neurology, Peter Kellaway Section of Neurophysiology, Baylor College of Medicine; Chief of Neurophysiology, Director of the Epilepsy and Neurophysiology Program, Texas Children's Hospital

James J Riviello Jr, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Up To Date Royalty Section Editor

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Reference Salary Employment

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Epileptic and epileptiform encephalopathies. EEG showing an epileptiform beta frequency burst.
EEG of a patient with Landau-Kleffner syndrome showing electrical status epilepticus of sleep (ESES).
Epileptic and epileptiform encephalopathies. Waking EEG in Landau-Kleffner syndrome, showing left posterior spikes.
Epileptic and epileptiform encephalopathies. EEG in Landau-Kleffner syndrome (LKS), before and after treatment with prednisone. The left EEG tracing shows electrical status epilepticus of sleep. The right tracing, obtained after 6 months of prednisone treatment, is normal.
Epileptic and epileptiform encephalopathies. Frequency-modulated auditory evoked response (FMAER), before and after treatment with prednisone. The left FMAER is absent. The right FMAER is normal following treatment.
 
 
 
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