Seizure Management

Status Epilepticus

Management of Convulsive Status Epilepticus

Use this as the emergency entry point: stabilize, give benzodiazepine therapy early, load a second-line ASM, and escalate to anesthetic infusion if seizures persist beyond 30 minutes.

ENLS 5.0 Protocol

1–5 min

Stabilize

ABCs, vitals, seizure onset time
IV access, ECG, finger-stick glucose
Treat hypoglycemia immediately with IV dextrose (or IM glucagon if no IV). Give thiamine before or with glucose when deficiency is suspected; never delay glucose.

5–10 min

Benzodiazepine

Lorazepam 0.1 mg/kg IV, max 4 mg; may repeat once
If no IV: midazolam 10 mg IM for adults; intranasal/buccal alternatives follow age- and weight-based protocol
Diazepam 0.15–0.2 mg/kg IV, max 10 mg

10–30 min

Load ASM

Fosphenytoin 20 mg PE/kg, max 1500 mg PE
Valproate 40 mg/kg, max 3000 mg
Levetiracetam 60 mg/kg, max 4500 mg

>30 min

Refractory SE

Intubate and start continuous anesthetic infusion
Midazolam or propofol infusion
Add second ASM and treat underlying cause

Clinical Reference Cards

Courtesy of Dr. Gena Ghearing

Ictal Interictal Continuum (IIC) Card Management Protocol

Status Epilepticus Pocket Reference Card

When does a seizure become status? t₁ and t₂

The “five minute rule” is not a rule about seizures in general — it is t₁ for convulsive status only. The ILAE 2015 operational definition sets two separate clocks, and they differ by seizure type:

t₁ — the point beyond which the seizure is unlikely to stop on its own. This is when emergency treatment starts.
t₂ — the point beyond which long-term consequences become likely: neuronal injury and death, and altered neuronal networks. This is what you are racing.

Type of status epilepticus	t₁ — treat now	t₂ — risk of lasting injury
Tonic–clonic (convulsive)	5 minutes	30 minutes
Focal with impaired awareness	10 minutes	> 60 minutes
Absence status	10–15 minutes	Unknown

Why this matters at the bedside: applying the convulsive five-minute threshold to every presentation is a common error in both directions. It starts the clock too early in absence status, where t₁ is 10–15 minutes and there is no established t₂; and it can create false reassurance in focal status with impaired awareness, which is often recognised late and where the injury window is measured in hours rather than the half hour people carry over from convulsive status.

Trinka E, Cock H, Hesdorffer D, et al. A definition and classification of status epilepticus — Report of the ILAE Task Force on Classification of Status Epilepticus. Epilepsia 2015;56(10):1515–23.

Detailed Time-Based Protocol

Phase	Time Range	Intervention & Dosing
Stabilization Phase	1–5 minutes	ABCs (Airway, Breathing, Circulation) Record seizure onset and monitor vitals Establish IV access ECG monitoring Check point-of-care blood glucose; treat hypoglycemia promptly (the protocol threshold is <60 mg/dL) Treat hypoglycemia immediately with IV dextrose (or IM glucagon without IV access). Add thiamine before or concurrently when deficiency is suspected; do not delay glucose.
Initial Therapy Phase	5–10 minutes	IV Lorazepam: 0.1 mg/kg, max 4 mg (may repeat once) OR Midazolam 10 mg IM for adults when IV access is not immediately available OR IV Diazepam: 0.15–0.2 mg/kg, max 10 mg (may repeat once)
Second-line Therapy	10–30 minutes	Fosphenytoin 20 mg/kg as phenytoin equivalents, infuse up to 150 mg PE per minute, maximum 1,500 mg; or Phenytoin 20 mg/kg, infuse up to 50 mg per minute. Continuous ECG and blood pressure monitoring. OR IV Valproic Acid: 40 mg/kg, max 3000 mg/dose, single dose OR IV Levetiracetam: 60 mg/kg, max 4500 mg/dose, single dose If none available, consider IV Phenobarbital: 15 mg/kg, single dose
Refractory Therapy	>30 minutes	Urgently involve neurocritical care; secure the airway when ongoing convulsions, impaired ventilation, or continuous-infusion therapy requires it Initiate continuous infusion therapy: Use a protocolized continuous infusion such as midazolam or propofol with continuous EEG and cardiorespiratory monitoring; loading, titration, treatment target, and duration must follow the local neurocritical-care protocol Add a second ASM (options: fosphenytoin, valproic acid, levetiracetam, lacosamide, or phenobarbital)
Breakthrough/Recurrence	N/A	Confirm recurrent electrographic seizure activity on raw EEG, reassess confounders and the treatment target, then titrate or change therapy using the local protocol Address underlying cause of seizures If super refractory SE, consider additional continuous infusion: Ketamine may be considered by a neurocritical-care team; dosing, contraindications, and monitoring vary by protocol and evidence base
Additional Therapies	N/A	Ketogenic diet Phenobarbital: 15–20 mg/kg Pentobarbital: 5–15 mg/kg then 0.5–5 mg/kg/h Etiology-directed immunotherapy when autoimmune or inflammatory status is suspected Epilepsy surgery Other rescue approaches such as therapeutic hypothermia or ECT have limited evidence and should be restricted to expert multidisciplinary consideration

Anti-Seizure Medications

Below is a rapid-reference list of anti-seizure medications (ASMs) with abbreviated adult epilepsy dosing, common adverse effects, and commonly reported laboratory intervals when applicable. Some entries are syndrome-specific, adjunctive, rescue, or off-label uses rather than interchangeable maintenance regimens.

Medication	Mechanism / Target	Abbreviated Adult Epilepsy Dosing	Common Side Effects	Common Laboratory Reference Range*
Acetazolamide	Carbonic anhydrase inhibitor	Oral: 375–1000 mg/day (divided doses)	Paresthesias, fatigue, taste alteration, acidosis, kidney stones	N/A
Brivaracetam	SV2A ligand — higher affinity and more selective than levetiracetam	Oral or IV: 50–200 mg/day (in 2 divided doses)	Drowsiness, dizziness, fatigue, irritability	N/A
Carbamazepine	Sodium channel blockade (fast inactivation)	Oral: 800–1200 mg/day (in 2–4 divided doses; range ~400–1600 mg)	Dizziness, drowsiness, diplopia, ataxia (HLA-B15:02 screening recommended before initiation for patients with ancestry in populations where HLA-B15:02 is common; consider HLA-A*31:01 risk according to ancestry and local guidance)	4–12 µg/mL
Cannabidiol (Dravet, LGS, or TSC-associated seizures)	Not fully defined — GPR55 antagonism, TRPV1 desensitisation, adenosine reuptake inhibition. Not a CB1 agonist	Oral: target 10 mg/kg/day for Dravet/LGS (maximum 20 mg/kg/day); target 25 mg/kg/day for TSC, divided BID	Diarrhea, fatigue, decreased appetite, somnolence	N/A
Cenobamate (new)	Dual: inhibits the persistent sodium current and positively modulates GABA-A at a non-benzodiazepine site	Oral: 200 mg/day (after gradual titration; max 400 mg/day)	Dizziness, somnolence, fatigue, headache, nausea	No established therapeutic target
Clobazam (adjunct for LGS)	1,5-benzodiazepine — positive allosteric GABA-A modulator (every other benzodiazepine is 1,4)	Oral: 10–40 mg/day (usually divided BID)	Sedation, drowsiness, drooling	Clobazam 30–300 ng/mL; N-desmethylclobazam 300–3000 ng/mL
Clorazepate	Benzodiazepine prodrug → nordiazepam; positive allosteric GABA-A modulator	Oral: 15–90 mg/day (divided doses)	Drowsiness, dizziness, fatigue, ataxia	N/A
Clonazepam (rarely used long-term)	Benzodiazepine — positive allosteric GABA-A modulator	Initial dose should not exceed 1.5 mg/day divided TID; titrate individually. Labeled maximum 20 mg/day.	Sedation, drowsiness, cognitive impairment, tolerance	N/A
Diazepam (Oral)	Benzodiazepine — positive allosteric GABA-A modulator	Oral: 4–40 mg/day (divided doses)	Sedation, fatigue, ataxia, muscle weakness	N/A
Eslicarbazepine acetate	Prodrug → eslicarbazepine; sodium channel blockade, stabilising the inactivated state	Oral: 800–1600 mg/day (usually once daily)	Dizziness, headache, diplopia, somnolence	N/A
Ethosuximide	T-type calcium channel blockade in thalamocortical relay neurons	Oral: start 500 mg/day and titrate; doses above 1500 mg/day require strict medical supervision (absence seizures)	Nausea, vomiting, lethargy, headache, weight loss	40–100 µg/mL
Everolimus (TSC associated seizures)	mTOR inhibitor — targets the pathway disrupted in tuberous sclerosis	Oral: Titrated to trough 5–15 ng/mL	Stomatitis, infections, rash, fatigue	5–15 ng/mL
Felbamate (rarely used – toxicity)	NMDA receptor antagonism (glycine site), plus sodium channel blockade and GABA-A potentiation	Oral: 1200–3600 mg/day (divided TID–QID)	Sedation, nausea, vomiting, risk of aplastic anemia/liver failure	N/A
Fenfluramine	Serotonin release and 5-HT receptor agonism (notably 5-HT2C), with sigma-1 receptor modulation	Oral solution: 0.1 mg/kg BID initially; up to 0.35 mg/kg BID (maximum 26 mg/day). Lower maximum with stiripentol plus clobazam.	Decreased appetite, somnolence, diarrhea, fatigue; boxed warning requires echocardiographic monitoring for valvular heart disease and pulmonary arterial hypertension	No established therapeutic target
Gabapentin (rarely effective for epilepsy)	Binds the alpha-2-delta subunit of voltage-gated calcium channels. Despite the name, not a GABA agonist	Oral: 900–3600 mg/day (divided TID)	Dizziness, somnolence, peripheral edema, ataxia	N/A
Ganaxolone (CDKL5 deficiency)	Neuroactive steroid — positive allosteric modulator of synaptic and extrasynaptic GABA-A receptors	Oral: Titrated to 600 mg TID (1800 mg/day)	Somnolence, pyrexia, salivary hypersecretion	N/A
Lacosamide	Enhances slow inactivation of sodium channels — a different action from the classic fast-inactivation blockers	Oral or IV: 200–400 mg/day divided BID; 600 mg/day was not more effective and caused more adverse reactions in trials	Dizziness, headache, nausea	10–20 mg/L
Lamotrigine	Sodium channel blockade with inhibition of glutamate release	Oral: 100–400 mg/day (in 2 divided doses; slow titration. Note that dosing changes for patients taking drugs that alter metabolism)	Rash (risk of Stevens–Johnson syndrome), dizziness, headache	3–15 µg/mL
Levetiracetam	Binds synaptic vesicle protein SV2A, modulating neurotransmitter release	Oral or IV: 1000–3000 mg/day divided BID; adjust for renal function	Drowsiness, dizziness, irritability, behavioral changes	10–40 µg/mL
Lorazepam	Benzodiazepine — positive allosteric GABA-A modulator; no active metabolite	Oral: 2–6 mg/day (divided doses)	Sedation, dizziness, weakness, unsteadiness	N/A
Methsuximide	Succinimide — T-type calcium channel blockade	Oral: 300–1200 mg/day	Nausea, vomiting, dizziness, drowsiness	10–40 µg/mL (as N-desmethylmethsuximide)
Midazolam (Nasal)	Benzodiazepine — positive allosteric GABA-A modulator; short acting	Nasal: 5 mg per dose (may repeat once)	Nasal discomfort, somnolence, runny nose	N/A
Oxcarbazepine	Prodrug → licarbazepine (MHD); sodium channel blockade	Oral: 600–2400 mg/day (divided BID)	Dizziness, sedation, hyponatremia	3–35 µg/mL (MHD)
Perampanel	Selective non-competitive AMPA receptor antagonist	Oral: 8–12 mg/day (once daily at bedtime)	Dizziness, somnolence, hostility, irritability, falls	No established therapeutic target
Phenobarbital	Barbiturate — prolongs GABA-A chloride channel opening; inhibits glutamate responses at higher concentrations	Oral or IV: 60–200 mg/day (usually once at bedtime)	Sedation, cognitive impairment, ataxia, dependence	10–40 µg/mL
Phenytoin	Use- and voltage-dependent sodium channel blockade (fast inactivation)	Oral or IV: 300–400 mg/day (divided BID; ~5–7 mg/kg/day to maintain level 10–20 µg/mL)	Nystagmus, ataxia, gingival hyperplasia, hirsutism, sedation	Total 10–20 µg/mL; free concentration is often more informative with low albumin, renal failure, pregnancy, or interacting drugs
Primidone (rarely used)	Metabolised to phenobarbital and PEMA, both active; GABA-A modulation	Oral: 750–1500 mg/day (divided BID–TID)	Sedation, ataxia, nausea, dizziness	N/A
Pregabalin (rarely used for epilepsy)	Binds the alpha-2-delta subunit of voltage-gated calcium channels	Oral: 150–600 mg/day (divided BID)	Dizziness, somnolence, weight gain, peripheral edema	N/A
Rufinamide (rare, LGS)	Prolongs the inactivated state of sodium channels	Oral with food: start 400–800 mg/day divided BID; titrate to a maximum of 3200 mg/day	Dizziness, fatigue, nausea, vomiting	N/A
Stiripentol (rare, Dravet)	Positive allosteric GABA-A modulator; also inhibits CYP, raising clobazam and norclobazam levels	Oral: 50 mg/kg/day divided BID or TID (maximum 3000 mg/day), used with clobazam for Dravet syndrome in the labeled population	Drowsiness, ataxia, loss of appetite	N/A
Tiagabine (rarely used)	Blocks the GAT-1 GABA reuptake transporter	Oral: 32–56 mg/day (divided BID–QID)	Dizziness, nervousness, fatigue, tremor	N/A
Topiramate	Multiple: sodium channels, GABA-A potentiation, AMPA/kainate antagonism, carbonic anhydrase inhibition	Oral: 100–400 mg/day (divided BID)	Cognitive slowing, weight loss, paresthesias, kidney stones	5–20 µg/mL
Valproate / Divalproex Sodium	Broad: sodium channels, T-type calcium channels, increased GABA turnover, histone deacetylase inhibition	Oral (DR/ER) or IV: 1000–3000 mg/day (divided BID–TID; ~15–60 mg/kg/day)	GI upset, tremor, weight gain, hair loss, hepatotoxicity, thrombocytopenia	50–125 µg/mL
Vigabatrin (restricted use; REMS)	Irreversible GABA-transaminase inhibitor, raising brain GABA	For refractory focal seizures: start 1000 mg/day divided BID; titrate to recommended 3000 mg/day	Visual field defects, sedation, irritability	N/A
Zonisamide	Sodium channels and T-type calcium channels, with weak carbonic anhydrase inhibition	Oral: 100–400 mg/day (once daily or divided BID)	Dizziness, somnolence, loss of appetite, weight loss	10–40 mcg/mL

*Laboratory ranges vary by assay and are not universal treatment targets. Clinical response, toxicity, sample timing, baseline concentration, interactions, protein binding, and free drug levels may matter more than a population interval. Doses are abbreviated educational examples; verify whether each use is labeled, adjunctive, syndrome-specific, or off-label.

Medication table for rapid educational reference only. Verify indication, formulation, interactions, organ-function adjustments, pregnancy considerations, titration, and current prescribing information before use.

ASM Flowcharts

These flow charts provide guidance on anti-seizure medication selection based on seizure type, mechanisms of action, and clinical applications:

Context: These 2021 figures are conceptual teaching aids, not current prescribing algorithms. Medication approval, pregnancy guidance, syndrome terminology, and comparative evidence change; verify the current label and guideline for the individual patient.

Choice of Anti-Seizure Medications

Monotherapy and add-on therapy options for seizures in adults and children:

Anti-seizure medication choice flowchart

Mechanisms of Action

Neurobiological targets of commonly used anti-seizure medications:

Clinical Spectrum of Anti-Seizure Medications

Treatment approaches for different types of epilepsy in adults and children:

Reference: Löscher, W., Klein, P. The Pharmacology and Clinical Efficacy of Antiseizure Medications: From Bromide Salts to Cenobamate and Beyond. CNS Drugs 35, 935–963 (2021). https://link.springer.com/article/10.1007/s40263-021-00827-8

ASM Withdrawal

ASM withdrawal should be performed gradually under medical supervision after careful consideration of seizure recurrence risk factors.

Key Considerations for ASM Withdrawal:

Use shared decision-making after an individualized review of epilepsy syndrome, seizure-free interval, prior course, treatment adverse effects, and consequences of recurrence
In adults seizure-free for 2 years, discuss that tapering may carry a higher long-term recurrence risk than continuing treatment; evidence does not establish one mandatory waiting period for everyone
In children seizure-free for 18–24 months, incorporate the syndrome's natural history and obtain an EEG when withdrawal is being considered
Choose a medication-specific taper; do not apply a universal 3–6 month schedule to every ASM
Discuss driving, employment, injury, pregnancy, and rescue-plan implications; follow current jurisdiction-specific driving rules during and after tapering

Use the prediction tool below to estimate seizure recurrence risk after medication withdrawal, but always consult your epilepsy specialist before making any medication changes.

Epilepsy Prediction Tools

Management of Refractory Epilepsy

Therapy Category	Description/Details
Definition	Drug-resistant epilepsy (DRE) is defined by failure of two tolerated, appropriately chosen and adequately used ASM schedules—whether alone or in combination—to achieve sustained seizure freedom. Referral to a comprehensive epilepsy center should occur promptly so the diagnosis, adherence barriers, epilepsy type, imaging, surgical candidacy, devices, dietary therapy, and psychosocial needs can be reviewed; referral does not commit a patient to surgery.
Surgical Options	Resection, lesionectomy, lobar/multilobar resections, or hemispherectomy in catastrophic cases; corpus callosotomy may reduce drop attacks.
Neuromodulation Techniques	VNS: Vagus nerve stimulation (VNS) has demonstrated that approximately 49% of patients achieve a ≥50% reduction in seizure frequency within 1–2 years (see VNS outcomes). RNS: Responsive neurostimulation (RNS) offers a median seizure reduction of around 60% over several years (see RNS outcomes). DBS: Deep brain stimulation (DBS) targeting the anterior nucleus of the thalamus has shown a median seizure reduction of about 56% in controlled trials (see DBS outcomes).
Dietary & Other Therapies	Ketogenic diet (or variants), immunotherapies, etc.
References	ILAE/AAN recommendations; ACNS guidelines; UpToDate; Epilepsy Foundation.

Pregnancy & Epilepsy

Most people with epilepsy can have a healthy pregnancy. Management should begin before conception when possible and balance seizure control, the risks of convulsive seizures, and medication-specific fetal risks. Do not stop an antiseizure medication abruptly during pregnancy.

Teratogenicity & Malformation Risks

Risk Level	Medications	Notes
High Risk	Valproate; also phenobarbital and topiramate when clinically feasible alternatives exist	Valproate has dose-dependent risk for major malformations (neural tube, cardiac) and adverse neurodevelopmental outcomes. The 2024 AAN/AES/SMFM guideline recommends avoiding valproate when clinically feasible; medication changes must still account for seizure type and seizure-control risk.
Intermediate	Carbamazepine, Phenytoin	Risk varies by medication and dose. Use the fewest medications and lowest effective doses compatible with seizure control rather than applying a blanket monotherapy rule.
Lowest Risk	Lamotrigine, Levetiracetam, Oxcarbazepine	The 2024 guideline recommends considering these when appropriate for the person’s epilepsy to minimize major congenital-malformation risk. No medication is universally safest for every epilepsy.

Historical Registry Snapshot

Do not use this older table as a current counseling calculator. It reproduces selected results from 2006–2012 publications with different enrollment, comparator, dose, and outcome methods. Current counseling should use the 2024 AAN/AES/SMFM guideline and the latest pregnancy-registry publications. The historical data remain useful for illustrating dose dependence and why estimates differ among registries.

Medication	NAAPR (Hernandez-Diaz 2012)	UK Register (Morrow 2006)	EURAP (Tomson 2011)
Lamotrigine	2.0%	3.2%	2.0% (<300mg) 4.5% (≥300mg)
Levetiracetam	2.4%	0% (small sample)	-
Carbamazepine	3.0%	2.2%	3.4% (<400mg) 8.7% (≥1000mg)
Phenytoin	2.9%	3.7%	-
Valproate	9.3%	6.2%	5.6% (<700mg) 24.2% (≥1500mg)
Topiramate	4.2%	7.1%	-
Phenobarbital	5.5%	-	5.4% (<150mg) 13.7% (≥150mg)
Unexposed / Control	1.1%	3.5%	-

Contraception

Interactions: Carbamazepine, phenytoin, phenobarbital, primidone, and higher-dose topiramate can reduce exposure to some hormonal contraceptives; estrogen-containing contraception can also lower lamotrigine concentrations.

Recommendation: Select contraception with the patient and prescribing clinicians using an interaction checker. IUDs avoid hepatic enzyme-induction interactions; other methods require individualized review.

Folic Acid

Current guideline floor: prescribe at least 0.4 mg folic acid daily before conception and during pregnancy for anyone treated with an ASM.

Higher doses: the optimal dose is uncertain. Prior neural-tube defect, nutritional factors, and medication choice warrant individualized maternal-fetal-medicine and neurology guidance rather than an automatic 4 mg rule.

ASM Monitoring

Clearance: Significantly increases for Lamotrigine (>50% drop), Levetiracetam, and Oxcarbazepine.

Action: Establish an individual pre-pregnancy clinical and concentration baseline when useful, then monitor symptoms and levels at a frequency determined by the medication, trimester, seizure risk, and rate of change.

Delivery & Postpartum

Labor: treat an ongoing convulsive seizure promptly using the institution’s pregnancy-aware acute-seizure protocol while addressing airway, fetal/maternal status, and obstetric causes such as eclampsia.

Postpartum: if doses were increased during pregnancy, make a medication-specific reduction plan before delivery and monitor for toxicity as clearance returns toward baseline. Avoid fixed taper schedules across all ASMs.

Breastfeeding

Generally safe and encouraged. Infant serum levels are typically low despite presence in milk. Monitor for sedation if on Phenobarbital/Primidone.

Primary guidance: AAN/AES/SMFM practice guideline on teratogenesis, perinatal, and neurodevelopmental outcomes after in-utero ASM exposure (2024). This section supports counseling and does not replace individualized neurology and maternal-fetal-medicine care.