01Approach to the Critical Patient/attcp34

Status epilepticus recognition

›Status epilepticus criteria

›Focal seizure with impaired awareness lasting >10 minutes

›Two seizures without return to baseline between events

›Failure to return to neurologic baseline within 30 to 60 minutes postictal

›Nonconvulsive status epilepticus — persistent confusion with subtle automatisms

Immediate stabilization priorities

›Airway and positioning

›Lateral decubitus position to reduce aspiration risk during postictal state

›Suction available at bedside

›Supplemental oxygen for SpO2 < 94%

›If unable to protect airway, definitive airway management

›Circulation

›IV access placement bilaterally

›Point-of-care glucose — immediate mandatory step in all patients

›If glucose < 3.0 mmol/l, dextrose 50% 50 mL IV immediately

›If thiamine deficiency risk, thiamine 100 mg IV before dextrose

›Monitoring bundle

›Continuous cardiac monitoring — arrhythmia as seizure mimic or consequence

›Continuous pulse oximetry

›Blood pressure every 5 minutes during active seizure or postictal period

›Neurologic reassessment every 15 minutes until return to baseline

Escalation triggers

›Red flags requiring immediate escalation

›Seizure duration >5 minutes — initiate benzodiazepine protocol

›Recurrent seizures without recovery — status epilepticus protocol

›Persistent altered consciousness beyond 60 minutes postictal

›New focal neurologic deficits — emergent CT head

02History/hx59

Seizure semiology

›Ictal features from witness account

›Behavioral arrest and staring without responsiveness

›Automatisms — oral (lip smacking, chewing), manual (picking, fumbling)

›Duration of seizure event — typically 1 to 2 minutes for focal impaired awareness

›Head deviation or eye turning — lateralizing value to contralateral hemisphere

›Unilateral limb posturing or clonic movements

›Secondary generalization — focal to bilateral tonic-clonic evolution

›Aura characteristics

›Epigastric rising sensation — most common aura in temporal lobe epilepsy

›Deja vu or jamais vu — highly localizing to mesial temporal lobe

›Olfactory or gustatory hallucinations — temporal lobe origin

›Fear or anxiety without external trigger

›Visual disturbances — formed or unformed depending on lobe of origin

›Postictal period

›Confusion and disorientation duration — typically minutes

›Amnesia for the event — characteristic of focal impaired awareness seizures

›Todd's paralysis — transient unilateral weakness implying contralateral focus

›Aphasia — suggests left temporal or dominant hemisphere focus

›Headache and fatigue

Triggers and context

›Precipitating factors

›Sleep deprivation

›Alcohol use or recent alcohol withdrawal

›Missed antiseizure medication doses

›Febrile illness

›Menstrual cycle correlation — catamenial epilepsy pattern

›Substance use — cocaine, methamphetamine as proconvulsants

03Physical Exam/exam35

Vital signs and general

›Stability snapshot

›Temperature — fever suggests CNS infection, encephalitis, or febrile provocation

›Blood pressure — hypertension raises concern for posterior reversible encephalopathy syndrome or eclampsia

›Heart rate — tachycardia postictal versus arrhythmia as primary event

›Respiratory rate and oxygen saturation

›Point-of-care glucose — must be documented early

Neurologic examination

›Mental status

›Level of consciousness and orientation — postictal versus encephalopathic baseline

›Language assessment — aphasia suggests left temporal or dominant focus

›Memory registration and recall

›Cranial nerves

›Visual fields — homonymous hemianopia from temporal or parietal lesion

›Papilledema — raised intracranial pressure

›Pupillary size and reactivity

›Motor system

›Pronator drift — subtle lateralizing weakness

›Todd's paralysis — transient unilateral weakness, resolves within 24 hours

›Babinski sign — upgoing plantar response suggesting corticospinal involvement

›Facial droop or asymmetry

›Reflexes

›Deep tendon reflexes — asymmetry as lateralizing sign

›Clonus if present

Seizure-specific findings

›Tongue examination

›Lateral tongue bite — highly suggestive of epileptic seizure

›Tip-of-tongue bite — more consistent with psychogenic nonepileptic seizure

04Differential Diagnosis/ddx45

Seizure mimics

›Syncope variants

›Convulsive syncope — brief irregular jerks, rapid recovery within seconds to 1 minute

›Cardiogenic syncope — arrhythmia as primary event

›ICD-10: R55 — syncope and collapse

›Psychogenic nonepileptic seizures

›Eye closure during event — suggests PNES over epilepsy

›Waxing and waning motor activity without clear offset

›Prolonged duration typically >3 minutes

›Slow or dramatic postictal recovery

›May coexist with true epilepsy in up to 10% of cases

›ICD-10: F44.5 — conversion disorder with seizures

›Transient ischemic attack

›Negative symptoms predominate — weakness, numbness, speech arrest without impaired awareness

›No postictal confusion

›ICD-10: G45.9 — TIA unspecified

›Transient global amnesia

›Isolated memory disturbance without automatisms or impaired responsiveness

›Repetitive questioning is characteristic

›ICD-10: G45.4 — transient global amnesia

›Migraine with aura

›Longer aura duration 20 to 60 minutes versus seizure aura seconds to minutes

›Followed by headache phase

›ICD-10: G43.1 — migraine with aura

Epilepsy type differentiation

›Absence seizures

›Brief 5 to 30 second duration without postictal confusion

›Generalized 3 Hz spike-wave on EEG distinguishes from focal impaired awareness

05Laboratory Tests/lt41

Immediate point-of-care tests

›Bedside glucose

›Mandatory in every patient with seizure

›Target threshold — glucose < 3.0 mmol/l requires immediate correction

›Hypoglycemia as both seizure cause and consequence

Basic metabolic panel

›Electrolytes

›Sodium — hyponatremia most common metabolic seizure provoker

›Calcium and magnesium — hypocalcemia and hypomagnesemia as seizure triggers

›Potassium for medication safety before starting antiseizure drugs

›Renal function — dose adjustment for renally cleared antiseizure medications

›Glucose

›Confirm quantitative result to complement point-of-care value

›Persistent hyperglycemia — hyperosmolar state as seizure provoker

Specialized seizure workup labs

›Serum prolactin

›Sensitivity approximately 78% when drawn 10 to 20 minutes post-seizure

›Elevated prolactin supports epileptic seizure over PNES

›Normal value does not exclude epileptic seizure — limited specificity

›Clinical utility primarily to support PNES when normal in appropriate context

›Antiseizure medication levels

›In known epilepsy — medication levels identify noncompliance as seizure trigger

›Phenytoin, carbamazepine, valproate, levetiracetam levels available

›Subtherapeutic levels suggest noncompliance or pharmacokinetic interaction

›Complete blood count

›If infection suspected as precipitant

›Baseline before starting valproate or carbamazepine due to hematologic side effects

›Hepatic function panel

06Diagnostic Tests/dt69

Scoring Systems

›ILAE 2017 seizure classification framework

›Focal onset — arises from network in one hemisphere

›Focal with impaired awareness — previously termed complex partial seizure

›Focal to bilateral tonic-clonic — formerly secondarily generalized

›Awareness preserved versus impaired distinguishes simple from complex partial

›Recurrence risk after first unprovoked seizure

›Overall risk of second seizure approximately 30% at 1 year; up to 50% at 2 years

›High recurrence risk factors — abnormal EEG, structural brain lesion, prior brain insult, nocturnal seizure

›Low recurrence risk — normal EEG, normal MRI, no identifiable risk factor

›Treatment recommended when recurrence risk exceeds benefit-risk threshold for medication

›PNES versus epilepsy clinical clues

›Ictal eye closure — 96% specificity for PNES over epileptic seizure

›Lateral tongue bite — specificity >90% for epileptic seizure

›Prolactin elevation — sensitivity 78%, specificity approximately 70% for epileptic seizure

›Gold standard is video-EEG monitoring capturing typical event

Electroencephalography

›EEG indications and timing

›All patients with first unprovoked seizure — ACEP Level B recommendation

›Highest diagnostic yield within 24 to 48 hours of event — captures postictal slowing and interictal discharges

›Can be safely delayed if treatment does not depend on immediate result

›Ambulatory EEG for outpatient workup when inpatient not feasible

›EEG findings in focal impaired awareness seizures

›Interictal temporal lobe spikes — 50 to 60% sensitivity in single routine EEG

›Postictal focal slowing over seizure focus

›Ictal temporal theta or delta with focal onset — seen during captured event

›Generalized 3 Hz spike-wave excludes focal onset; suggests absence epilepsy

›Continuous EEG monitoring

›Indicated if persistent altered consciousness after clinical seizure termination

›Identifies nonconvulsive status epilepticus — major diagnostic pitfall in ICU patients

MRI

›MRI brain indications

›All patients with suspected focal-onset seizure should undergo MRI

›Superior to CT for epilepsy-specific pathology

›Up to 30% of first seizure patients have abnormalities on MRI versus approximately 10% with CT alone

›Epilepsy protocol MRI specifications

›Thin coronal FLAIR sequences through hippocampi — 1 to 3 mm slice thickness

›T1 3D volumetric sequence for cortical thickness analysis

›T2 axial through temporal lobes

›DWI — acute cortical diffusion restriction in status epilepticus or ischemia

›Gadolinium contrast for tumor, abscess, or inflammatory lesion

›Key MRI findings in focal epilepsy

›Hippocampal sclerosis — T2 hyperintensity and volume loss, most common structural cause of temporal lobe epilepsy

›Focal cortical dysplasia — cortical thickening, blurring of gray-white junction, transmantle sign

›Low-grade glioma — T2 hyperintense mass without surrounding edema

›Cavernous malformation — blood products on gradient echo or susceptibility-weighted imaging

›Periventricular heterotopia — nodular gray matter along lateral ventricle walls

›MRI timing

›Emergent if new focal deficits, persistent altered consciousness, or acute structural lesion suspected

›Elective epilepsy-protocol MRI if initial emergency CT normal and patient returned to baseline

CT

›CT head without contrast indications

›First seizure in adults — emergent CT indicated per standard of care

›Focal-onset seizure with any neurologic deficit

›Fever with seizure to exclude abscess or hemorrhage before LP

›Head trauma, anticoagulant use, malignancy, or immunocompromise

›Failure to return to neurologic baseline — excludes hemorrhage, herniation

›CT limitations in epilepsy

›Sensitivity for hippocampal sclerosis — very low; requires MRI

›Misses focal cortical dysplasia, small cavernomas, low-grade gliomas

›Detection rate for acute findings approximately 10% in first seizure population

›Normal CT does not exclude structural epileptogenic lesion

›CT angiography

›Consider if arteriovenous malformation suspected — acute bleed with pulsatile lesion on non-contrast CT

›Not routine in focal seizure workup

Ultrasound

›Bedside ultrasound applications in seizure evaluation

›Cardiac echo — structural heart disease as cause of syncope versus seizure

›Optic nerve sheath diameter >5 mm — bedside marker of raised intracranial pressure

›Aortic assessment in unexplained syncope or cardiovascular presentation

›Point-of-care ultrasound limitations

›No direct diagnostic role for seizure diagnosis

›Does not image brain parenchyma in adults

›Useful adjunct for hemodynamic assessment in unstable postictal patient

07Disposition/dispo26

Admission criteria

›Indications for inpatient admission

›Failure to return to neurologic baseline within 30 to 60 minutes postictal

›Status epilepticus — any duration meeting criteria

›Recurrent seizures during observation period without full recovery between events

›New focal neurologic deficits on examination

›Acute structural lesion on imaging — hemorrhage, ischemic stroke, tumor, abscess

›Suspected CNS infection — fever, nuchal rigidity, immunocompromise

›Inability to arrange timely outpatient EEG and MRI

›Waxing and waning consciousness suggestive of nonconvulsive status epilepticus

ICU-level care criteria

›ICU transfer triggers

›Refractory status epilepticus requiring continuous infusion therapy

›Hemodynamic instability or respiratory failure requiring ventilation

›Acute elevated intracranial pressure with herniation risk

›Continuous EEG monitoring required for suspected nonconvulsive status epilepticus

Discharge criteria

›Safe discharge requirements

›Return to neurologic baseline

›Normal or non-acute CT if obtained

›No acute provoking factor requiring inpatient treatment

›Safe home environment with responsible adult available

›Reliable follow-up arranged with neurology within 1 to 2 weeks

›Driving restrictions counseled and documented

›Return precautions provided

Observation consideration

›Observation unit indications

›First seizure with borderline features requiring extended reassessment

08Treatment/t86

Acute seizure management

›First aid and positioning

›Lateral decubitus position — reduces aspiration risk

›Do not restrain during active seizure — injury prevention

›Clear surrounding objects

›Do not place objects in mouth

›Time seizure duration from onset

›Benzodiazepine protocol for seizure >5 minutes

›First-line — midazolam 10 mg IM for adults (>40 kg)

›Non-inferior to IV lorazepam in prehospital trials (RAMPART trial)

›Preferred when IV access not yet established

›Alternative — lorazepam 4 mg IV over 2 minutes

›Repeat once after 5 minutes if no response

›Maximum 8 mg total IV lorazepam

›Alternative — diazepam 10 mg IV or 10 to 20 mg rectal

›Rectal route for out-of-hospital use

›If no IV access and IM not available — intranasal midazolam 10 mg

Second-line antiseizure medications

›Fosphenytoin IV

›Loading dose 20 mg phenytoin equivalents per kg IV

›Maximum rate 150 mg PE per minute

›Monitor for hypotension and cardiac arrhythmia during infusion

›Cardiac monitoring mandatory during infusion

›Maintenance 4 to 6 mg PE per kg per day in divided doses

›Levetiracetam IV

›Loading dose 60 mg/kg IV up to 4500 mg

›Infused over 15 minutes

›Preferred in patients with hepatic dysfunction, or where phenytoin contraindicated

›Well tolerated; minimal drug interactions

›Maintenance 1000 to 3000 mg daily in 2 divided doses

›Valproate IV

›Loading dose 40 mg/kg IV up to 3000 mg

›Infused over 10 minutes

›Avoid in pregnancy and women of childbearing potential

›Contraindicated in mitochondrial disease and hepatic failure

›Maintenance 15 to 45 mg/kg daily in divided doses

›Lacosamide IV

›Loading dose 400 mg IV infused over 30 to 60 minutes

›Used when other second-line agents have failed

›Cardiac monitoring required — PR interval prolongation risk

›Maintenance 200 to 400 mg daily in 2 divided doses

Refractory status epilepticus management

›Anesthetic agents for refractory status epilepticus

›Propofol IV continuous infusion

›Initiation 1 to 2 mg/kg IV bolus then 1 to 4 mg/kg per hour infusion

›Titrate to burst suppression on EEG

›Monitor for propofol infusion syndrome with prolonged high-dose use

›Midazolam IV continuous infusion

›Loading 0.2 mg/kg IV then 0.05 to 0.5 mg/kg per hour

›Titrate to seizure suppression on continuous EEG

›Phenobarbital IV

›Loading 15 to 20 mg/kg at 50 to 100 mg per minute

›Respiratory depression risk — intubation often required

›Ketamine IV

›Emerging agent in super-refractory status epilepticus

›1 to 2 mg/kg IV bolus then 0.5 to 5 mg/kg per hour infusion

Long-term antiseizure medication initiation

›Decision to treat after first unprovoked seizure

›Not mandatory after a single event with low recurrence risk

›Shared decision-making with patient and family

›Treatment recommended if abnormal EEG, structural lesion, nocturnal onset, prior brain insult, or patient preference

›Lamotrigine — preferred for long-term focal epilepsy management

›SANAD II trial — superior treatment retention over levetiracetam and zonisamide for focal epilepsy

›Starting dose 25 mg daily (without enzyme inducers)

›Slow titration over 4 to 6 weeks required

›Target 100 to 200 mg daily in 2 divided doses

›Risk of rash — Stevens-Johnson syndrome; slow titration essential

›Drug interactions — valproate doubles lamotrigine levels; enzyme inducers halve levels

›Levetiracetam — preferred when rapid titration needed

›Starting dose 250 mg twice daily

›Increase by 500 mg every 1 to 2 weeks

›Target 1000 to 2000 mg daily in 2 divided doses

›Psychiatric side effects — irritability, anxiety, mood changes; monitor closely

›Renal dose adjustment required for CrCl < 50 mL/min

›Minimal drug interactions — advantage in polypharmacy

›Carbamazepine and oxcarbazepine

›Effective alternative agents for focal epilepsy

›Enzyme-inducing — multiple pharmacokinetic drug interactions

›Carbamazepine starting 100 to 200 mg twice daily; target 600 to 1200 mg daily

›Hyponatremia risk — particularly with oxcarbazepine

›HLA-B*1502 screening before use in patients of Asian ancestry — Stevens-Johnson risk

Reversible cause correction

›Metabolic correction

›Sodium replacement for hyponatremia — gradual correction to prevent osmotic demyelination

›Magnesium replacement for hypomagnesemia

›Calcium replacement for hypocalcemia

›Correction of hyperthermia

›Medication and substance triggers

›Reinstate missed antiseizure medication doses

›Alcohol withdrawal seizure management — benzodiazepine taper protocol

›Avoid prescribing seizure threshold-lowering medications

09Special Populations/sp63

Pregnancy

›Eclampsia — priority diagnosis in any pregnant or postpartum seizure

›Blood pressure >140/90 mmHg in pregnancy with seizure is eclampsia until proven otherwise

›Magnesium sulfate first-line agent for eclamptic seizure

›Loading dose 4 to 6 g IV over 15 to 20 minutes

›Maintenance infusion 1 to 2 g per hour

›Monitor for toxicity — respiratory depression, loss of DTRs, cardiac arrest

›Definitive treatment — delivery of fetus after maternal stabilization

›Teratogenicity considerations

›Valproate — avoid in women of childbearing potential

›Major malformations up to 10% of exposed pregnancies

›Neurodevelopmental delay in up to 40% of exposed children

›Neural tube defects, cognitive impairment

›Lamotrigine — preferred antiseizure medication in pregnancy

›Lower teratogenic risk than valproate or phenobarbital

›Levels drop significantly during pregnancy due to increased renal clearance — monitor levels and dose accordingly

›Levetiracetam — acceptable in pregnancy; also requires level monitoring

›Folic acid 5 mg daily — all women of childbearing potential on antiseizure medications

›Pharmacokinetic changes in pregnancy

›Increased renal clearance reduces antiseizure medication levels — levels may need doubling

›Monthly drug level monitoring throughout pregnancy recommended

›Breastfeeding generally safe with lamotrigine and levetiracetam

›Contraception interactions

›Enzyme-inducing antiseizure medications — carbamazepine, phenytoin, phenobarbital — reduce oral contraceptive efficacy

›Recommend non-hormonal contraception or higher-dose preparations

Geriatric

›Epidemiology in older adults

›Incidence of epilepsy highest after age 65 — second peak of bimodal distribution

›Cerebrovascular disease most common etiology in elderly

›Metabolic causes more common than in younger adults — hyponatremia, hyperglycemia, drug interactions

›Atypical presentation in elderly

›Prolonged postictal confusion mimicking dementia exacerbation or delirium

›Subtle automatisms without overt motor manifestations

›Todd's paralysis mimicking acute stroke — critical diagnostic pitfall

›Falls as sole presentation of seizure event

›Medication considerations in elderly

›Levetiracetam — preferred due to minimal drug interactions

›Start at half the standard dose — 250 mg once daily

›Psychiatric side effects may be more pronounced in elderly

›Lamotrigine — acceptable but slower titration required

›Avoid phenobarbital — excessive sedation and cognitive effects

›Avoid carbamazepine if cardiac conduction disease present

›Renal dose adjustment for levetiracetam in all elderly with reduced CrCl

›Polypharmacy risk

›High drug-drug interaction risk with antiseizure medications in elderly

›Enzyme-inducing drugs affect anticoagulation, cardiac medications, statins

›Falls risk increases with sedating antiseizure medications

Pediatrics

›Age-specific considerations

›Complex febrile seizures — focal features or duration >15 minutes warrant further workup

›Infantile spasms — not focal onset; ACTH treatment required; distinct from complex partial

›Childhood absence epilepsy — brief staring spells; 3 Hz spike-wave; distinct management

›Focal epilepsy in children

›Benign childhood epilepsy with centrotemporal spikes — most common childhood focal epilepsy

›Often does not require treatment — spontaneous remission typical by adolescence

›Seizures typically nocturnal or during drowsiness

›Focal cortical dysplasia — important structural cause requiring MRI epilepsy protocol

›Pediatric dosing of acute antiseizure medications

›Midazolam IM — 0.2 mg/kg per dose (maximum 10 mg)

›Lorazepam IV — 0.1 mg/kg per dose (maximum 4 mg)

›Diazepam rectal — 0.5 mg/kg (maximum 20 mg)

›Levetiracetam IV — 60 mg/kg loading dose (maximum 4500 mg)

›Long-term pediatric antiseizure medication

›Oxcarbazepine — preferred for focal epilepsy in children

›Levetiracetam — weight-based dosing 20 to 60 mg/kg daily in 2 doses

›Valproate — use with caution under age 2 due to hepatotoxicity risk

10Background/b55

Epidemiology

›Prevalence and incidence

›Epilepsy affects approximately 50 million people worldwide

›Focal epilepsy accounts for approximately 60% of all epilepsy cases

›Temporal lobe epilepsy is the most common form of focal epilepsy in adults

›Annual incidence approximately 50 per 100,000 population

›Age distribution

›Bimodal distribution — peak incidence in young children and adults over 65

›First unprovoked seizure in adults — about one-third experience a second seizure within 1 year; nearly half within 2 years

›Approximately 70% of patients with epilepsy achieve seizure remission with appropriate antiseizure medication

›Prognosis and outcomes

›Recurrence risk above 60% if structural lesion identified on MRI

›SUDEP — sudden unexpected death in epilepsy — higher risk with uncontrolled focal to bilateral tonic-clonic seizures

›Significant psychosocial impact — driving restrictions, employment limitations, psychiatric comorbidity

›Depression and anxiety present in up to 50% of patients with temporal lobe epilepsy

Pathophysiology

›Seizure generation mechanisms

›Focal impaired awareness seizures arise from a restricted epileptogenic network in one hemisphere

›Impaired awareness results from propagation to bilateral hemispheres disrupting default mode network and ascending arousal system

›Temporal lobe seizures most commonly arise from hippocampal or parahippocampal circuits

›Hippocampal sclerosis — neuronal loss and gliosis in CA1, CA3, and dentate gyrus regions

›Propagation and secondarization

›Focal to bilateral tonic-clonic evolution requires spread through corpus callosum and subcortical structures

›Postictal suppression — widespread cortical inhibition following seizure; responsible for postictal confusion and Todd's paralysis

›Ictal hyperperfusion followed by postictal hypoperfusion in seizure focus

›Underlying structural etiologies

›Hippocampal sclerosis — most common cause of drug-resistant temporal lobe epilepsy; associated with prolonged febrile seizures in childhood

›Focal cortical dysplasia — abnormal cortical development; highly epileptogenic

›Low-grade glioneuronal tumors — DNET, ganglioglioma — characteristically epileptogenic

›Cavernous malformations — blood products cause cortical irritation; perilesional siderosis

›2017 ILAE etiologic classification

›Structural — hippocampal sclerosis, cortical dysplasia, tumor, vascular malformation

›Genetic — channelopathies, familial focal epilepsy syndromes

›Infectious — HSV encephalitis, neurocysticercosis

›Immune — autoimmune encephalitis — NMDA receptor, LGI1, CASPR2 antibodies

›Metabolic — pyridoxine deficiency, glucose transporter deficiency

›Unknown — largest category in clinical practice

Therapeutic Considerations

›First-line antiseizure medication selection principles

›Focal epilepsy — lamotrigine or levetiracetam preferred based on SANAD II trial

›Drug selection considers seizure type, comorbidities, pharmacokinetics, teratogenicity, and tolerability

›Monotherapy preferred — polypharmacy increases side effects and drug interactions

›Drug-resistant focal epilepsy

›Defined as failure of 2 appropriately dosed and tolerated antiseizure medications

›Affects approximately 30% of focal epilepsy patients

›Referral to epilepsy center for surgical candidacy evaluation is standard of care

›Temporal lobectomy in appropriately selected mesial temporal sclerosis patients — 60 to 80% seizure-free at 2 years

›Surgical considerations

›Resective surgery — removal of seizure focus when MRI-visible lesion concordant with EEG

›Laser interstitial thermal therapy — minimally invasive alternative for mesial temporal sclerosis

›Vagus nerve stimulation — palliative 50% seizure reduction in approximately 50% of drug-resistant patients

›Responsive neurostimulation — closed-loop system detecting and aborting seizures

›Lifestyle modifications

›Sleep hygiene — sleep deprivation is a major modifiable trigger

›Alcohol avoidance or minimization — well-established seizure trigger

›Medication compliance — most common preventable cause of breakthrough seizures

›Ketogenic diet — considered for drug-resistant epilepsy; stronger evidence in pediatrics

›Caffeine in excess may lower seizure threshold

11Patient Discharge Instructions/pdi34

copy discharge instructions

›What happened and what to expect

›You were evaluated for a seizure — a brief episode where your brain had abnormal electrical activity

›After a focal seizure, confusion and fatigue for hours is normal and expected

›You may not remember the seizure itself — this is typical and does not indicate a serious problem

›Driving restrictions

›You must not drive until cleared by your doctor — laws vary by province and state but typically require 3 to 12 months seizure-free before driving is permitted

›Inform your family members and caregivers of this restriction

›Contact your provincial motor vehicle authority if you hold a commercial driving license

›Activity restrictions

›Avoid swimming alone until seizure control is established

›Avoid working at heights or operating heavy machinery

›Take showers rather than baths to reduce drowning risk

›Avoid situations where a sudden loss of consciousness would be dangerous

›Medications

›Take your antiseizure medication exactly as prescribed — do not miss doses

›Do not stop your medication without speaking to your neurologist — abrupt discontinuation can trigger seizures

›Watch for rash if started on lamotrigine — especially in the first 8 weeks; return to ER if rash develops

›Watch for mood changes, irritability, or depression if started on levetiracetam

›Lifestyle guidance

›Get adequate sleep every night — sleep deprivation is a major seizure trigger

›Minimize alcohol consumption — alcohol is a well-established seizure trigger

›Avoid recreational drugs

›Stay hydrated — avoid severe dehydration

›Follow-up

›Neurology appointment within 1 to 2 weeks — contact your family doctor or the neurology clinic directly

›EEG (brainwave test) will be arranged as an outpatient

›MRI of the brain may be arranged if not completed in the emergency department

12References/r36

Guidelines and key sources

›ILAE 2017 classification of seizure types and epilepsies

›International League Against Epilepsy — operational classification of seizure types

›Focal with impaired awareness replaces complex partial seizure terminology

›Smith PEM — Initial Management of Seizure in Adults — NEJM 2021

›Comprehensive review of first seizure management, workup, and recurrence risk

›https://www.nejm.org/doi/full/10.1056/NEJMcp2024526

›Gavvala JR, Schuele SU — New-Onset Seizure in Adults and Adolescents — JAMA 2016

›Evidence-based framework for evaluation of new-onset seizure

›https://jamanetwork.com/journals/jama/fullarticle/10.1001/jama.2016.18625

›Marson A et al — SANAD II trial — Lancet 2021

›Lamotrigine superior treatment retention for focal epilepsy versus levetiracetam and zonisamide

›https://pubmed.ncbi.nlm.nih.gov/33838757

›Pellinen J et al — Improving Epilepsy Diagnosis Across the Lifespan — Lancet Neurology 2024

›Current approaches to epilepsy diagnosis including imaging and EEG

›https://pubmed.ncbi.nlm.nih.gov/38631767

›Neligan A et al — Prognosis After First Unprovoked Seizure — Cochrane 2023

›Systematic review of recurrence risk and prognostic factors

›https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD013847.pub2/full

›Kanner AM, Bicchi MM — Antiseizure Medications for Adults With Epilepsy — JAMA 2022

›Review of antiseizure medication selection, efficacy, and tolerability

›https://jamanetwork.com/journals/jama/fullarticle/10.1001/jama.2022.3880

›Blumenfeld H — Impaired Consciousness in Epilepsy — Lancet Neurology 2012

›Pathophysiology of consciousness impairment in focal seizures

›https://pubmed.ncbi.nlm.nih.gov/22898735

›Asadi-Pooya AA et al — Adult Epilepsy — Lancet 2023

›Comprehensive review of adult epilepsy including epidemiology and treatment

›https://pubmed.ncbi.nlm.nih.gov/37459868

Evidence & Review

Evidence & Review