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Summary Table

Domain	Details
Risk Factors	Family history of epilepsy, prior febrile seizures, history of CNS infection (meningitis, encephalitis), perinatal injury (hypoxic-ischemic encephalopathy), traumatic brain injury, cortical dysplasia, stroke, brain tumor, neurodegenerative disease, alcohol/drug withdrawal
Etiology	Structural (tumor, vascular malformation, cortical dysplasia), genetic (channelopathies, Dravet syndrome, juvenile myoclonic epilepsy), infectious (neurocysticercosis, HSV encephalitis), metabolic (uremia, hepatic encephalopathy, hypoglycemia, hyponatremia), immune-mediated (anti-NMDA receptor encephalitis), unknown
Patient Presentation	Recurrent unprovoked seizures. May present with witnessed tonic-clonic activity, episodes of staring and unresponsiveness, involuntary jerking of a limb, or unexplained episodes of confusion with amnesia for the event
Classic Physical Exam	Post-ictal confusion and drowsiness, tongue bite (lateral tongue bite is highly suggestive), urinary incontinence, Todd paralysis (transient focal weakness after a focal or generalized seizure). Exam may be entirely normal between events
Key Diagnostic Results	EEG showing epileptiform discharges (spikes, sharp waves, spike-and-wave complexes). MRI brain showing structural lesion if present. Prolactin level elevated within 20 minutes of a generalized tonic-clonic or focal seizure with impaired awareness (helps distinguish from psychogenic nonepileptic events)
Management	Antiseizure medications (ASMs) as first-line. Drug selection is guided by seizure type: levetiracetam or lamotrigine for focal onset; valproate or levetiracetam for generalized onset. Status epilepticus requires IV benzodiazepines as the immediate first step
Keywords	"Unprovoked seizure," "post-ictal confusion," "tongue bite," "rhythmic jerking," "staring spells," "EEG with spike-and-wave," "Todd paralysis," "aura preceding seizure"

1. Pathophysiology

Epilepsy results from an imbalance between excitatory and inhibitory neurotransmission in the cerebral cortex. At its core, the disease reflects excessive neuronal synchronization and hyperexcitability. Under normal conditions, GABAergic inhibitory interneurons provide a counterbalance to glutamatergic excitatory signaling. In epilepsy, this balance tips in favor of excitation through a variety of mechanisms: gain-of-function mutations in sodium or calcium channels (prolonging depolarization), loss-of-function mutations in potassium or GABA receptor channels (reducing repolarization and inhibition), or structural disruptions to cortical circuitry (such as cortical dysplasia or hippocampal sclerosis) that create abnormal excitatory loops.

Focal seizures originate from a discrete cortical focus. The clinical manifestation depends entirely on the location of this focus. A seizure arising from the motor cortex produces contralateral rhythmic jerking. A seizure in the temporal lobe produces an aura (often described as a rising epigastric sensation, deja vu, or fear), followed by behavioral arrest and oral automatisms. This is the direct link between anatomy and symptoms that test writers exploit: the clinical description tells you where the seizure starts.

Generalized seizures involve bilateral cortical networks from onset. Absence seizures result from abnormal oscillatory activity in thalamocortical circuits, producing the characteristic 3 Hz spike-and-wave discharges on EEG and the abrupt onset/offset staring spells without post-ictal confusion. Generalized tonic-clonic seizures involve widespread cortical activation, first producing tonic stiffening (sustained depolarization) followed by clonic jerking (rhythmic cycles of depolarization and repolarization), then a prolonged post-ictal phase reflecting neuronal exhaustion and transient cortical suppression.

Epileptogenesis refers to the process by which a normal brain becomes prone to seizures after an initial insult. After a traumatic brain injury or stroke, for example, the surrounding brain tissue undergoes gliosis, loss of inhibitory interneurons, and sprouting of aberrant excitatory connections. This creates a hyperexcitable network that can generate spontaneous seizures weeks to years later. This explains why there is often a latent period between a brain insult and the first seizure, and why a new-onset seizure in an older adult should prompt urgent evaluation for a structural lesion such as a tumor or stroke.

2. Classification and Clinical Manifestation

The International League Against Epilepsy (ILAE) classification is the framework used on exams. The first determination is seizure onset type, which drives all downstream decisions.

Seizure Classification by Onset

Onset Type	Subtype	Key Clinical Features
Focal Onset	Aware (simple partial)	Consciousness preserved. Motor (clonic jerking of one limb), sensory (tingling, visual phenomena), autonomic (flushing, tachycardia), or psychic (deja vu, fear) symptoms depending on cortical focus
	Impaired Awareness (complex partial)	Consciousness impaired. Behavioral arrest, staring, oral or manual automatisms (lip smacking, picking at clothes). Often arises from the temporal lobe. Followed by post-ictal confusion
	Focal to Bilateral Tonic-Clonic	Begins focally then generalizes. Patient may report an aura before losing consciousness. Previously called "secondarily generalized"
Generalized Onset	Absence	Abrupt onset and offset staring lasting 5 to 30 seconds. No post-ictal confusion. Can be provoked by hyperventilation. EEG shows 3 Hz generalized spike-and-wave. Typically in children ages 4 to 10
	Myoclonic	Brief, shock-like jerks of the extremities, often bilateral and symmetric. Consciousness preserved. Common in juvenile myoclonic epilepsy (JME), often occurring shortly after awakening
	Tonic	Sustained stiffening of the trunk and extremities. Consciousness impaired. Common in Lennox-Gastaut syndrome
	Clonic	Rhythmic bilateral jerking without a preceding tonic phase
	Tonic-Clonic	Tonic phase (stiffening, forced expiration producing a cry, apnea) followed by clonic phase (rhythmic jerking). Post-ictal confusion, tongue bite, urinary incontinence
	Atonic	Sudden loss of muscle tone ("drop attacks"). Brief. Common in Lennox-Gastaut syndrome
Unknown Onset	Epileptic spasms	Clusters of brief flexor or extensor spasms. Characteristic of infantile spasms (West syndrome). EEG shows hypsarrhythmia. Onset typically between 3 and 12 months of age

Selected Epilepsy Syndromes

Syndrome	Age of Onset	Seizure Types	EEG Pattern	Key Associations
Childhood Absence Epilepsy	4 to 10 years	Absence	3 Hz spike-and-wave	Normal intelligence, provoked by hyperventilation, responds to ethosuximide or valproate
Juvenile Myoclonic Epilepsy (JME)	12 to 18 years	Myoclonic, tonic-clonic, sometimes absence	4 to 6 Hz polyspike-and-wave	Morning myoclonus, triggered by sleep deprivation and alcohol, lifelong treatment usually needed, responds to valproate or levetiracetam
West Syndrome (Infantile Spasms)	3 to 12 months	Epileptic spasms	Hypsarrhythmia	Developmental regression, treat with ACTH or vigabatrin (vigabatrin preferred if due to tuberous sclerosis)
Lennox-Gastaut Syndrome	1 to 7 years	Multiple types (tonic, atonic, atypical absence)	Slow spike-and-wave (< 2.5 Hz)	Intellectual disability, refractory to treatment, often preceded by West syndrome
Dravet Syndrome	< 1 year	Prolonged febrile seizures progressing to multiple seizure types	Generalized and multifocal discharges	SCN1A mutation, worsened by sodium channel blockers (carbamazepine, phenytoin), developmental regression

3. Diagnostic Workup

Test	Role	Key Findings
EEG	Best initial test for evaluating seizure type and epilepsy syndrome	Interictal epileptiform discharges (spikes, sharp waves). 3 Hz spike-and-wave in absence epilepsy. Focal slowing or spikes in focal epilepsy
MRI Brain	Best initial imaging test; most sensitive for structural lesions	Hippocampal sclerosis (mesial temporal sclerosis), tumors, cortical dysplasia, vascular malformations, prior infarcts
Prolonged Video-EEG Monitoring	Gold standard for seizure characterization and localization	Captures clinical and electrographic events simultaneously. Essential for pre-surgical evaluation and differentiating epileptic from nonepileptic events
Serum Prolactin	Adjunct to distinguish epileptic seizure from psychogenic nonepileptic event	Elevated (greater than twice baseline) within 10 to 20 minutes of a generalized tonic-clonic or focal seizure with impaired awareness. Not elevated in psychogenic events or absence seizures
Basic Labs	Rule out provoked (acute symptomatic) seizures	Glucose, electrolytes (sodium, calcium, magnesium), BUN/creatinine, hepatic function, toxicology screen
Lumbar Puncture	Only if CNS infection or autoimmune encephalitis is suspected	CSF pleocytosis in infectious etiologies; anti-NMDA receptor antibodies in autoimmune encephalitis

The first step after a witnessed seizure is to determine whether the seizure was provoked or unprovoked. This distinction is foundational. A provoked seizure (due to hypoglycemia, hyponatremia, alcohol withdrawal, or acute drug intoxication) does not warrant a diagnosis of epilepsy and does not require long-term antiseizure medication. Basic laboratory studies including glucose, a comprehensive metabolic panel, and a toxicology screen should be obtained in every patient presenting with a first seizure.

EEG is the best initial test for evaluating the type and etiology of seizures. A routine 20- to 40-minute EEG captures interictal epileptiform discharges in approximately 50% of patients with epilepsy on the first study. If the initial EEG is normal, sleep-deprived EEG increases the diagnostic yield. The EEG pattern often determines the diagnosis: 3 Hz generalized spike-and-wave points to childhood absence epilepsy, while focal temporal sharp waves suggest temporal lobe epilepsy. Be aware that a normal EEG does not rule out epilepsy; it only means that no epileptiform activity was captured during the recording window.

MRI of the brain is indicated in virtually all patients with new-onset seizures, except in children with a classic presentation of childhood absence epilepsy or benign rolandic epilepsy. MRI is superior to CT in detecting cortical dysplasia, hippocampal sclerosis, low-grade tumors, and cavernous malformations. In the acute setting (emergency department), a non-contrast CT may be obtained first to rapidly rule out hemorrhage or a large mass, but MRI is always the preferred imaging modality when epilepsy is suspected.

Prolonged video-EEG monitoring is reserved for patients in whom the diagnosis is uncertain (to differentiate epileptic seizures from psychogenic nonepileptic events) or for pre-surgical evaluation in drug-resistant epilepsy. This is the gold standard for correlating clinical behavior with electrographic activity.

4. Management and Treatment

First-Line Antiseizure Medications

Seizure Type	First-Line ASM Options	Important Notes
Focal onset (aware or impaired awareness)	Levetiracetam, lamotrigine, oxcarbazepine, carbamazepine	Carbamazepine and oxcarbazepine can worsen generalized epilepsies
Generalized tonic-clonic	Valproate, levetiracetam, lamotrigine	Valproate is highly effective but avoided in women of childbearing age due to teratogenicity
Absence	Ethosuximide (first choice for absence-only epilepsy), valproate	Ethosuximide does not treat tonic-clonic seizures; if both coexist, use valproate or lamotrigine
Myoclonic (e.g., JME)	Valproate, levetiracetam	Avoid carbamazepine, phenytoin, and gabapentin (can worsen myoclonic and absence seizures)
Infantile spasms	ACTH, vigabatrin	Vigabatrin preferred if etiology is tuberous sclerosis
Lennox-Gastaut	Valproate, lamotrigine, clobazam, rufinamide	Often refractory; multiple drugs and adjunctive therapies may be needed

Status Epilepticus Management

Time Point	Step	Agent and Dose
0 to 5 minutes	Stabilize (ABCs, check glucose, position)	Supportive care. Administer thiamine + glucose if indicated
5 to 20 minutes	First-line: Benzodiazepine	IV lorazepam 0.1 mg/kg (max 4 mg per dose, may repeat once) OR IM midazolam 10 mg (if no IV access) OR rectal diazepam 0.2 mg/kg
20 to 40 minutes	Second-line: IV antiseizure medication	IV fosphenytoin 20 mg PE/kg, OR IV levetiracetam 60 mg/kg (max 4500 mg), OR IV valproate 40 mg/kg
> 40 minutes (refractory)	Third-line: Anesthetic agents, ICU admission	IV midazolam infusion, IV propofol, or IV pentobarbital with continuous EEG monitoring

After a first unprovoked seizure, the decision to start an antiseizure medication is nuanced. A single unprovoked seizure carries a recurrence risk of approximately 40% to 50% over 2 years. Treatment is recommended when the recurrence risk is high: abnormal EEG with epileptiform discharges, structural lesion on MRI, nocturnal seizure, or a prior brain insult (remote symptomatic etiology). After two or more unprovoked seizures separated by more than 24 hours, the diagnosis of epilepsy is established and treatment is indicated, as the recurrence risk exceeds 60%.

Drug selection depends on seizure type, patient age, sex, and comorbidities. For focal epilepsy, levetiracetam and lamotrigine are the most commonly used first-line agents due to their favorable side-effect profiles and lack of significant drug interactions. Carbamazepine remains effective but carries a risk of hyponatremia and Stevens-Johnson syndrome (especially in patients with HLA-B*1502, common in Southeast Asian populations). For generalized epilepsy, valproate is highly effective across seizure types (tonic-clonic, absence, myoclonic) but is contraindicated in pregnancy due to neural tube defects and neurodevelopmental harm. In women of childbearing age, levetiracetam or lamotrigine is preferred.

A critical exam concept: certain ASMs can worsen certain seizure types. Carbamazepine, oxcarbazepine, phenytoin, and gabapentin can exacerbate absence and myoclonic seizures. This is a frequently tested trap. If a patient with JME (myoclonic jerks + generalized tonic-clonic seizures) is started on carbamazepine and the myoclonus worsens, the next best step is to switch to valproate or levetiracetam.

Status epilepticus is defined as continuous seizure activity lasting 5 minutes or longer, or two or more seizures without return to baseline. The immediate first step is always IV benzodiazepine (lorazepam is preferred intravenously). This is one of the most tested management sequences in medical licensing exams. If benzodiazepines fail, the second-line agent is an IV loading dose of fosphenytoin, levetiracetam, or valproate. Refractory status epilepticus (failure of first- and second-line agents) requires ICU admission and continuous infusion of an anesthetic agent with continuous EEG monitoring.

Medication withdrawal may be considered after 2 or more seizure-free years, but this decision requires careful risk stratification. The risk of recurrence after withdrawal is higher in patients with an abnormal EEG, structural brain lesion, or juvenile myoclonic epilepsy (which typically requires lifelong treatment).

Surgical evaluation is indicated for drug-resistant epilepsy, defined as failure of two appropriately chosen and adequately dosed ASMs. The most common and most successful epilepsy surgery is anterior temporal lobectomy for mesial temporal lobe epilepsy with hippocampal sclerosis. Pre-surgical evaluation includes prolonged video-EEG, high-resolution MRI, neuropsychological testing, and sometimes PET, SPECT, or intracranial EEG.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Syncope (vasovagal or cardiac)	Can produce brief tonic posturing or myoclonic jerks ("convulsive syncope"), urinary incontinence. Witness may describe "seizure-like" activity	Preceded by lightheadedness, pallor, diaphoresis, or triggered by prolonged standing. Recovery is rapid (seconds) with no post-ictal confusion. Brief myoclonic jerks in syncope are irregular, not sustained rhythmic clonic activity
Psychogenic Nonepileptic Events (PNEE)	Can mimic tonic-clonic seizures with dramatic motor activity. May be prolonged. May not respond to benzodiazepines	Eyes are typically closed during the event (in epileptic seizures, eyes are usually open). Asynchronous, side-to-side head movements. Pelvic thrusting. No post-ictal elevation of prolactin. Normal EEG during the event on video-EEG monitoring
Transient Ischemic Attack (TIA)	Can produce focal neurological symptoms that resolve	TIA produces negative symptoms (weakness, numbness, vision loss). Focal seizures produce positive symptoms (rhythmic jerking, tingling, visual flashing). TIA does not cause rhythmic motor activity
Migraine with aura	Can produce visual phenomena, sensory symptoms, and confusion	Migraine aura evolves slowly over 5 to 60 minutes and is followed by headache. Epileptic visual aura is brief (seconds) and often consists of simple colored shapes or flashing lights, not the scintillating scotoma of migraine
Hypoglycemia	Can cause confusion, altered consciousness, diaphoresis, and even seizures	Check blood glucose. Seizures due to hypoglycemia are provoked and resolve with glucose correction. Does not represent epilepsy
Parasomnias (sleepwalking, night terrors)	Nocturnal events with abnormal behavior and amnesia	Occur from non-REM sleep (first third of the night), duration is minutes, no stereotyped motor patterns. Frontal lobe epilepsy seizures are brief (< 1 minute), stereotyped, and can occur multiple times per night
Breath-holding spells (pediatric)	Child loses consciousness and may have tonic posturing after a trigger (crying, minor injury)	Always provoked by pain, frustration, or crying. Cyanotic or pallid appearance. Self-limited. No epileptiform discharges on EEG

6. Traps and High-Yield Pearls

The single most common way students lose points on epilepsy questions is by failing to classify the seizure type before selecting a drug. The vignette will describe a clinical event, and the correct answer depends entirely on whether the seizure is focal or generalized. If you pick carbamazepine for a patient who actually has juvenile myoclonic epilepsy (a generalized syndrome), you will make the patient worse, and that is exactly the wrong answer the test writer designed. Always classify first, then treat.

A second frequent trap involves the first seizure scenario. Many students reflexively choose to start an antiseizure medication after a single unprovoked seizure, but the correct answer depends on risk stratification. If the EEG is normal, MRI is normal, and the neurological exam is normal, observation without medication is a valid and often tested correct answer.

The status epilepticus sequence is tested repeatedly. The first step is always a benzodiazepine. Students who jump to phenytoin or levetiracetam as the initial therapy will get it wrong. The question will sometimes frame the scenario such that the patient has been seizing for "over 5 minutes" or "arrives to the emergency department with ongoing seizure activity." This is your cue: give the benzodiazepine first.

Watch for the psychogenic nonepileptic event disguised as refractory seizures. A vignette describing a patient who has "seizures" unresponsive to multiple medications, with closed eyes during the event, and a normal EEG, is pointing you toward PNEE, not drug-resistant epilepsy. The next best step is video-EEG monitoring, not adding another medication.

Finally, be alert to the teratogenicity question. A young woman with epilepsy who is planning pregnancy or discovers she is pregnant will appear in a vignette. Valproate must be avoided (neural tube defects, cognitive impairment in offspring). The correct answer is to switch to lamotrigine or levetiracetam and ensure adequate folic acid supplementation. Never abruptly discontinue an ASM in a pregnant patient, as uncontrolled seizures pose their own risks to the fetus.

The core competency tested across epilepsy questions is your ability to classify the seizure, match it to the correct drug, recognize status epilepticus, and identify when the presentation is not epilepsy at all.

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