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Continuing Education Activity

Ethosuximide is a central nervous system agent used to treat absence epilepsy, and this educational session equips healthcare professionals with the necessary information for delivering targeted and personalized care. This activity outlines the indications, actions, and contraindications for ethosuximide, providing essential information for its effective application in clinical settings. The mechanism of action, adverse event profile, dosing guidelines, monitoring requirements, and relevant interactions of ethosuximide are thoroughly reviewed. A review of this pharmacological information assists healthcare professionals in crafting tailored treatment plans that meet individual patient needs, optimizing therapeutic outcomes while minimizing potential adverse reactions. The discussion focuses on enhancing informed decision-making among healthcare providers during ethosuximide administration. Additionally, this activity highlights the interprofessional healthcare team's crucial role in effectively managing ethosuximide therapy.


  • Evaluate the mechanism of action of ethosuximide.

  • Identify the indications for ethosuximide therapy.

  • Assess the most common adverse drug reactions associated with ethosuximide therapy.

  • Implement effective collaboration and communication among interprofessional team members to improve outcomes and treatment efficacy for patients who might benefit from ethosuximide therapy.


Ethosuximide is FDA-approved for the management of absence seizures in patients 3 or older.[1] Additionally, several studies have suggested ethosuximide may also have some analgesic effects, making it a potential therapy for neuropathic pain.[2][3]

FDA-Approved Indications

Ethosuximide has demonstrated level A evidence for managing childhood absence seizures and has been effectively used to treat this condition since the 1960s.[4][5] A 2010 trial demonstrated that ethosuximide and valproic acid were more effective than lamotrigine for treating absence seizures.[6] The seizure freedom rates with initial ethosuximide and valproic acid treatment were 53% and 58%, respectively. These patients were then followed for 12 months to evaluate their long-term outcomes. This study data was published in 2013 and demonstrated ethosuximide has better tolerability than valproic acid.[7] Ethosuximide has similar efficacy compared to valproic acid in adolescent patients.[8] 

Due to its effectiveness and relatively limited adverse event profile, ethosuximide is considered the first-line therapy for absence epilepsy. If absence seizures are refractory to ethosuximide monotherapy, valproic acid can be added to increase the probability of seizure control.[9] While ethosuximide is effective for absence seizures, it is typically reserved solely for this condition. Ethosuximide has demonstrated no benefit in symptomatic epilepsies or other generalized epilepsies. Valproic acid is recommended over ethosuximide as initial monotherapy for patients with concurrent generalized tonic-clonic (GTC) seizures, as ethosuximide does not help control GTC seizures and can potentially exacerbate them.

Off-Label Uses

The International League Against Epilepsy (ILAE) recommends ethosuximide for treating neurodevelopmental delay with generalized epilepsy (NDD with generalized epilepsy). This type of epilepsy is characterized by generalized seizure activity along with neurodevelopmental delays and responds well to medications like valproate, ethosuximide, or lamotrigine. The ILAE consensus highlights the importance of selecting appropriate treatments based on the specific phenotypes and genetic characteristics of sodium channel neuron 8A (SCN8A)-related disorders. The ILAE recommends valproic acid as the initial treatment for epilepsy with eyelid myoclonia (EEM), a condition previously known as Jeavons syndrome. There is moderate consensus regarding the efficacy of ethosuximide and clobazam in treating this condition. Levetiracetam or lamotrigine are preferred alternatives for women of childbearing age. However, additional randomized controlled trials are required.[10][11]

Mechanism of Action

Ethosuximide (3-ethyl-3-methyl pyrrolidine-2,5-dione) is a succinimide agent with anticonvulsant properties. Phensuximide and methsuximide, the other 2 succinimides, have less favorable adverse effect profiles and lower efficacy than ethosuximide.[12] This drug class was first studied in the 1950s using mouse models.

Thalamocortical neurons are thought to use low-threshold T-type calcium channels to generate the classic 3 Hz "spike-and-wave" discharges associated with absence seizures. Ethosuximide can reduce the threshold of T-type calcium currents and disrupt the oscillatory activity of thalamocortical circuitry by blocking T-type calcium channels.[13]


Absorption: Ethosuximide's bioavailability exceeds 90%.

Distribution: Ethosuximide demonstrates negligible protein binding, readily crosses the blood-brain barrier, and has a distribution volume of approximately 0.7 L/kg.[14]

Metabolism: Ethosuximide is metabolized hepatically (80%) into inactive metabolites, primarily by CYP3A4 enzymes.[15]

Elimination: Approximately 10% to 20% of ethosuximide is excreted unchanged in the urine. If the patient's creatinine clearance falls below 10 mL/min, the dose should be decreased by 25%. Caution is advised when administering ethosuximide to patients with hepatic impairment, though no dose adjustments have been defined for these patients. Ethosuximide has a relatively long half-life: 30 hours in children and 50 to 60 hours in adults. Because of its long half-life, ethosuximide can take 7 to 10 days to reach steady state.


Available Dosage Forms and Strengths

Ethosuximide is administered using 250 mg capsules or a 250 mg/5 mL oral suspension. The oral suspension demonstrates faster absorption than the capsules.

Adult Dosing

The typical adult ethosuximide dose is 500 mg orally once daily. This daily dose may be increased by 250 mg every 4 to 7 days to a maximum daily dose of 1500 mg.

Specific Patient Populations

Hepatic impairment: The product labeling does include dosage adjustments for patients with hepatic impairment. Ethosuximide should be used cautiously for these patients.

Renal impairment: No dosage adjustment is necessary for patients with a creatinine clearance (CrCl) greater than 30 mL/min. For patients with CrCl less than 30 mL/min, ethosuximide should be administered cautiously using low initial doses.[16] Patients on hemodialysis may require additional doses before or after their sessions to maintain therapeutic levels.[16]

Pregnancy considerations: Ethosuximide is a category C drug (possibly unsafe in pregnancy) known to cross the placenta. Serum concentrations of ethosuximide in neonates are comparable to that of mothers receiving ethosuximide.[17] Ethosuximide should be used as monotherapy at the lowest effective dose possible during pregnancy. Ethosuximide levels should be obtained before the patient becomes pregnant and monitored during pregnancy. The American Academy of Neurology (AAN), American Epilepsy Society (AES), and Society for Maternal-Fetal Medicine (SMFM) 2024 guidelines advise that women who are pregnant (or may become pregnant) with epilepsy on antiseizure medications (including ethosuximide) should be informed of the limited data on pregnancy-related outcomes associated with these drugs.[18]

Breastfeeding considerations: Ethosuximide can be excreted in breast milk, making breastfeeding while taking ethosuximide potentially hazardous. Transfer rates can reach 25%-30% of maternal levels. Close monitoring is recommended for infants exposed to ethosuximide through breast milk. No specific adverse effects have been linked solely to exposure to this medication, but observed adverse effects include drowsiness, impaired feeding, and developmental delays, particularly in younger or exclusively breastfed infants. The potential for additive effects with other maternal anticonvulsants should be considered. Obtaining the infant's serum ethosuximide level can assuage or confirm concerns regarding infant exposure or potential toxicity.[19] 

Pediatric patients: According to the American Academy of Neurology (AAN), ethosuximide or valproic acid are the first-line treatment options for reducing seizure frequency in patients with childhood absence epilepsy.[20] Dosing should start at 125 mg twice daily for children aged 3 to 6. Children 6 or older and adults can be administered 250 mg twice daily. The total daily dose may be increased by 250 mg every 4 to 7 days to 20 mg/kg, divided into twice daily dosing. The dosing and serum concentrations of ethosuximide demonstrate a linear relationship. When discontinuing, ethosuximide should be tapered slowly as abrupt withdrawal may cause absence status epilepticus.

Older patients: Ethosuximide is effective for absence seizures in children, but there is limited data on its long-term efficacy and safety in older adults. Agranulocytosis and drug-induced neutropenia have been reported.[21]

Adverse Effects

The overall incidence of adverse effects associated with ethosuximide therapy is lower compared to most other anti-seizure medications (ASMs).[22] Gastrointestinal adverse effects (eg, nausea, vomiting, diarrhea, anorexia) are common initially and often diminish within 2 weeks. Other common adverse effects include drowsiness, lethargy, insomnia, and hiccups. Headache may occur in 14% of children taking ethosuximide. 

Documented rare idiosyncratic reactions include Stevens-Johnson syndrome, agranulocytosis, aplastic anemia, and systemic lupus erythematosus. If idiosyncratic reactions occur, ethosuximide should be discontinued. Full recovery may take some time following discontinuation.[23][24] Drug-induced lupus erythematosus is characterized by anti-histone and antinuclear antibodies.[25] Priapism has been reported infrequently.[26]

Drug-Drug Interactions

  • Enzyme-inducing ASMs such as phenytoin, carbamazepine, and phenobarbital can reduce serum concentrations of ethosuximide by accelerating its elimination.[27] Valproic acid has various effects on ethosuximide concentrations.[28][29][30][31] 
  • Ethosuximide may increase phenytoin levels, but it has no enzyme-inducing properties. 
  • Isoniazid may reduce ethosuximide metabolism, while rifampicin can increase ethosuximide clearance.[32][33]
  • One study indicated that ethosuximide significantly reduced lamotrigine serum concentrations based on patient age. Specifically, children and adolescents treated with ethosuximide showed a 37% reduction in lamotrigine levels compared to 14% in adults.[34]


Patients with hypersensitivity to succinimide medications should avoid taking ethosuximide.

Warnings and precautions

  • Ethosuximide should be administered cautiously to patients with hepatic disease, as dosing adjustments for patients with these conditions are undefined.
  • Antiseizure medications such as ethosuximide increase the risk of suicidal thoughts or behaviors. Patients receiving ethosuximide should be monitored for depression, suicidal ideation, or unusual changes in mood or behavior.[35][36]
  • Ethosuximide can cause drug-induced immune thrombocytopenia (DITP). [37] DITP typically occurs 1 to 3 weeks after initiation, with recurrence within 24 hours upon re-challenge. Platelet counts may drop by 3,000/mm³. Management involves discontinuation, monitoring platelet counts, and considering antiplatelet antibody assessment. Ethosuximide should be avoided in patients with a history of ethosuximide-induced DITP.


There are no guidelines for therapeutic drug monitoring of ethosuximide. Any ethosuximide dosage adjustment should be based on the patient's clinical response and electroencephalography (EEG) results. Ethosuximide levels are monitored by measuring the patient's trough levels. The therapeutic concentration for ethosuximide ranges from 40 to 100 μg/mL. Patients with absence status epilepticus may require concentrations above 120 μg/mL to achieve seizure control.[14] A dimple HPLC-UV method has been developed for therapeutic drug monitoring (TDM) of ethosuximide and other ASM levels. This method allows for the simultaneous determination of ethosuximide alongside several other ASMs and metabolites and requires only 100 µL of human plasma that may be prepared using a simple process. The dimple HPLC-UV is practical for pediatric, pregnant, older, and critically ill patients.[38]

A complete blood count (CBC) and liver function tests (LFTs) can also be obtained intermittently to monitor for severe but rare hematologic dyscrasias (eg, pancytopenia, agranulocytosis, leukopenia). However, no evidence suggests this is sufficient to alert physicians of a severe idiosyncratic reaction. The pattern of serum enzyme elevations is typically mixed cholestatic-hepatocellular. Any ethosuximide-induced liver injury resolves quickly after discontinuing and typically recurs promptly after re-exposure.[15]


Signs and Symptoms of Overdose

Studies using mouse models suggest the earliest symptom of ethosuximide toxicity is ataxia. Toxic patients can progress to dyspnea, respiratory failure, and death.[39] In cases of acute ethosuximide overdose in humans, clinical features may include nausea, vomiting, central nervous system depression, and coma with respiratory depression.

Management of Overdose

There is no antidote for ethosuximide toxicity. Recommendations involve observation in an emergency room or inpatient setting.[40] Treatment typically involves the administration of activated charcoal and supportive care. Hemodialysis can safely and effectively clear ethosuximide from the body.[41][42]

Enhancing Healthcare Team Outcomes

Primary care clinicians are commonly the first medical care providers to be informed about staring episodes or poor school performance. These symptoms suggest absence seizures, prompting a referral to neurology. After diagnosing absence epilepsy and initiating ethosuximide, both primary care physicians and neurologists should monitor for clinical benefit from ethosuximide therapy. If a patient remains seizure-free for longer than 2 years while on ethosuximide, and if the patient's EEG has normalized, the medication may be slowly tapered over weeks to see if the patient has developed terminal remission. A pediatric neurologist should be consulted for seizures refractory to ethosuximide. 

Ethosuximide is the most effective treatment for new-onset childhood absence epilepsy. However, initial monotherapy fails in 47% of cases. One pharmacokinetic study involving 211 participants revealed that area under the curve (AUC) levels of 1,027 and 1,489 μg·h/mL correspond to a 50% and 75% probability of seizure freedom, respectively. Monte Carlo simulations recommend daily doses of 40 and 55 mg/kg. Dosage adjustments based on body weight can enhance the success of the treatment.[43]

Ethosuximide therapy requires an interprofessional healthcare team, including clinicians, nursing staff, pharmacists, and mental health professionals. Nursing can counsel on medications and the disease state and serve as a liaison between other disciplines. Pharmacists should verify dosing, check for potential drug-drug interactions, and guide administration. Specialists may also offer their opinions and work with the prescribing clinicians to ensure the patient receives the appropriate therapeutic interventions. An interprofessional team approach and communication among clinicians (MDs, DOs, NPs, PAs), neurologists, pharmacists, and nurses are crucial to decreasing potential adverse effects, improving disease course and quality of life, and improving patient outcomes associated with ethosuximide.



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