Seizures and the first fit

A seizure is a transient occurrence of signs and symptoms produced by abnormal excessive or synchronous neuronal activity in the brain. The patient who has just had one, or who is still having one, is among the commonest neurological presentations to the emergency department, and the Fellowship candidate must do four things in order: stop the seizure if it is ongoing, exclude the rapidly reversible causes (glucose above all), decide whether the event was provoked or unprovoked — because that single distinction governs recurrence risk, antiepileptic drug initiation and driving — and arrange safe disposition with the right imaging, the right referral and the right counselling. A seizure that has not stopped at five minutes has crossed into status epilepticus and is managed up the benzodiazepine ladder (see the status epilepticus topic); the present topic covers everything else — the stopped seizure, the first fit, the workup and the advice.[1][2][3]

Definition and classification

An epileptic seizure is the transient neurological event — the clinical manifestation of the abnormal synchronous neuronal discharge. Epilepsy is the chronic tendency to have recurrent unprovoked seizures, and the International League Against Epilepsy gives a practical clinical definition: epilepsy is present with two or more unprovoked seizures more than 24 hours apart, or with a single unprovoked seizure and a probability of further seizures of at least 60 per cent over the next 10 years (which approximates the recurrence risk after two unprovoked seizures), or with a recognised epilepsy syndrome.[1] This definition matters in the emergency department because a first unprovoked seizure in an adult already carries a recurrence risk high enough to trigger driving restrictions and a workup even before a second event — the candidate must not wait for the "second seizure" to act.

The classification that runs the rest of the topic is provoked versus unprovoked. [1]

Seizures are also classified by semiology, which guides the EEG and MRI interpretation by the neurologist rather than changing the emergency workup: focal aware (consciousness intact, formerly simple partial), focal impaired-awareness (formerly complex partial), focal-to-bilateral tonic-clonic (formerly secondary generalisation), and the generalised onset types — tonic-clonic, absence, myoclonic, atonic. A first presentation is most often a focal-to-bilateral tonic-clonic seizure because that is the event dramatic enough to bring the patient in. [1]

Epidemiology and recurrence risk

About one in ten people will have a seizure in their lifetime, and the annual incidence of a first unprovoked seizure is roughly 50 to 70 per 100,000. The Fellowship question is rarely "how common is it" and almost always "what is the chance of another one" — and the answer is now well quantified. A Cochrane synthesis of the prognosis after a first unprovoked seizure found a pooled recurrence of about 32 per cent at one year and 39 to 46 per cent at two years, falling to a low rate thereafter for those who remain seizure-free.[5]

The recurrence risk is not uniform, and four factors move it up — the AAN/AES guideline and the prognostic literature converge on them:[2][5]

A patient with two or three of these factors approaches a 60 per cent recurrence risk over the next two years — which is the threshold the ILAE uses to diagnose epilepsy after a single seizure. This is the arithmetic that justifies starting an antiepileptic drug after one seizure in selected patients, and the arithmetic the OSCE counselling station is built around.[1][2]

Pathophysiology

A seizure is sustained by excessive glutamatergic (excitatory) drive and a failure of GABAergic (inhibitory) control, producing a population of neurones that fire synchronously and recruit neighbouring cortex. The clinical semiology reflects the cortex involved — motor (tonic-clonic), sensory (aura), autonomic, or conscious awareness impaired (temporal). When the seizure terminates (most do so spontaneously within two minutes), a wave of neuronal exhaustion and inhibitory suppression produces the post-ictal state — confusion, amnesia, headache, sleepiness and sometimes a Todd paresis, a transient focal weakness lasting hours to a day or two that is a focal post-ictal inhibition and not a stroke. The pitfall is the reverse — labelling a genuine acute stroke as a Todd paresis — which is why any focal deficit that does not recover promptly is reimaged and treated as a stroke until proven otherwise. [1]

The recurrence risk has a structural correlate: a seizure from a chronic lesion (tumour, scar, malformation) recurs because the lesion persists, whereas a seizure from a transient provoking factor (hypoglycaemia, alcohol) does not recur once the factor is removed. This is the mechanistic basis of the provoked-versus-unprovoked distinction that organises the whole topic. [1]

Clinical presentation

Most first seizures are witnessed, and the history from a bystander is worth more than any scan. The generalised tonic-clonic seizure has an abrupt loss of consciousness, a tonic phase (stiffening, cry, cyanosis, upward eye deviation), a clonic phase (rhythmic limb jerking for one to two minutes), and a post-ictal phase (confusion, amnesia, sleepiness, headache). Lateral tongue-biting, urinary incontinence and post-ictal confusion favour a seizure over its mimics. A preceding aura (epigastric rising, déjà vu, olfactory hallucination, focal sensory disturbance) localises to a focal onset and raises the probability of an epileptogenic focus. The patient who arrives post-ictal is examined for a focal deficit (a Todd paresis or a structural lesion), head trauma, a rash or a needle mark, and the temperature (a febrile first seizure demands a search for infection including meningitis). [1]

Atypical presentations matter. In the elderly, seizures are more often focal, the post-ictal confusion is prolonged and may be misdiagnosed as delirium, and the cause is more often structural (stroke, tumour, subdural) or metabolic. In the known-epilepsy patient, the first question is adherence and the drug level — non-compliance is the commonest reason for a breakthrough. In the alcoholic, a seizure within 6 to 48 hours of cessation is an alcohol-withdrawal seizure, typically a single generalised convulsion that is self-limiting and not epilepsy. [1]

Differential diagnosis

Not everything that shakes is a seizure, and a misdiagnosis is doubly harmful — the patient gets unnecessary antiepileptic drugs and the true cause (cardiac, metabolic, psychogenic) goes untreated. Up to a third of patients referred to epilepsy services with "refractory seizures" have psychogenic non-epileptic seizures; the emergency department is where this mistake begins.[2]

The single highest-yield discriminator at the bedside is the post-ictal state: syncope recovers in under a minute, a seizure takes minutes to hours, and PNES has none. The second is the capillary glucose, which excludes hypoglycaemia in seconds. The third is the ECG, which exposes the cardiac cause masquerading as a seizure — a long QT, a Brugada pattern, a conduction block — and which is performed on every patient with a suspected first seizure. [1]

Bedside assessment

Assess in parallel, not in sequence. Airway and breathing — open the airway, position laterally (recovery position) once the cervical spine is cleared, suction secretions, give high-flow oxygen; bag-valve-mask ventilate if apnoeic. Circulation — IV access, blood pressure and heart rate, a fluid bolus if hypotensive. Disability — check the capillary glucose immediately (the single most important bedside test), examine the pupils, and document the Glasgow Coma Scale, reproduced here because it grades the post-ictal depth and is examined. The GCS sums three responses: Eye opening (4 spontaneous, 3 to voice, 2 to pain, 1 none), Verbal response (5 oriented, 4 confused, 3 inappropriate words, 2 incomprehensible sounds, 1 none), and Motor response (6 obeys commands, 5 localises pain, 4 withdraws, 3 abnormal flexion, 2 abnormal extension, 1 none), for a maximum of 15 and a minimum of 3 — record also the temperature and a focused neurological examination for a focal deficit. Exposure — look for head trauma, a MedicAlert bracelet, needle marks, a rash, and the tongue. Take the history from any witness: the onset, the duration, the motor pattern, the recovery, and the provoking context (alcohol, sleep deprivation, drugs, recent illness, head injury). [1]

If the patient is still seizing at five minutes, the assessment pivots to the status epilepticus ladder — give a benzodiazepine and start the clock (see the status epilepticus topic). The post-ictal patient who does not wake up is presumed to be in non-convulsive status until an EEG proves otherwise. [1]

Investigations

Investigations run in parallel with resuscitation and never delay the first drug in an ongoing seizure. In the stopped, stable first seizure they answer four questions: is there a reversible metabolic or toxic cause, is there a structural intracranial cause, is there an infective cause, and is there a cardiac cause masquerading as a seizure. [1]

A few specifics the Fellowship examiner tests. Non-contrast CT is the emergency-department structural study of choice because it is fast, available, and detects the haemorrhage, the mass effect and the large lesion; MRI is more sensitive (mesial temporal sclerosis, a small tumour, cortical dysplasia) but is deferred. An EEG performed within 24 to 48 hours of a first seizure is more likely to show an epileptiform abnormality and improves the recurrence-risk estimate; a normal interictal EEG does not exclude epilepsy. A toxicology screen is not routine — it is sent when the history or the examination suggests a toxin or withdrawal. A prolactin level, once popular to distinguish a seizure from a syncope or a PNES, is no longer recommended because it is non-specific. The ECG is the investigation most often omitted and most often diagnostic when a "seizure" is in fact a cardiac arrhythmia with secondary convulsive movements. [1]

Immediate management

ABCDE is the frame, and the glucose is the key. In the patient who has stopped seizing and is post-ictal, the priority is the airway (recovery position, suction, oxygen), the capillary glucose (treat if low — give 50 mL of 50 per cent dextrose IV in the adult, or 250 mL of 10 per cent dextrose in the child, and thiamine 100 mg IV before or with the glucose in the alcoholic or malnourished patient to prevent Wernicke encephalopathy), and the search for a provoking factor. A benzodiazepine is given only if the seizure is ongoing or recurs in the department — lorazepam 4 mg IV over two minutes (repeat once at 10 minutes), or midazolam 10 mg IM if IV access is impossible. A patient who has clearly stopped seizing and recovered does not need a benzodiazepine, and giving one to a post-ictal patient adds respiratory depression without benefit. If the seizure does not stop at five minutes, escalate to the status epilepticus ladder: a second benzodiazepine dose, then a second-line anti-seizure medication (fosphenytoin 20 mg PE/kg, levetiracetam 60 mg/kg, or valproate 30 mg/kg), then an anaesthetic infusion for refractory disease. [1]

Definitive management — starting the antiepileptic drug

The Fellowship candidate must know that an antiepileptic drug is not automatic after a first seizure. The decision to start lifelong medication balances the reduction in recurrence against the side effects, the teratogenicity, the interactions and the stigma — and the evidence says the trade-off is closer than it appears. The MESS trial randomised over 1400 patients with early epilepsy or a single seizure to immediate versus deferred antiepileptic treatment and found that immediate treatment delayed the time to the next seizure but did not improve long-term seizure remission at three to five years; a Cochrane synthesis confirmed this — immediate treatment reduces the one- to two-year recurrence risk but does not change the longer-term probability of being seizure-free, nor the quality of life.[3][4]

When the decision is to treat, the agent matters. [1]

Levetiracetam is the preferred first-line agent for a new adult diagnosis: it is broad-spectrum (covers focal and generalised seizures), has minimal drug interactions (renal excretion, no hepatic enzyme induction — important for the contraceptive pill, warfarin and other antiepileptics), is available intravenously, and is well tolerated. The oral dose starts at 500 mg twice daily (titrated to 1000 to 3000 mg/day), and an IV load of 20 to 60 mg/kg is used in status. Valproate is at least as effective but is avoided in women of childbearing potential because it is teratogenic (neural tube defects, facial clefts) and lowers the childhood IQ and raises the risk of autism; it carries prescribing restrictions under the pregnancy prevention programme. In the woman who might become pregnant, levetiracetam or lamotrigine is preferred, with folate supplementation and pre-conception neurology counselling. Phenytoin is largely historical for new-onset treatment (interactions, gingival hypertrophy, narrow therapeutic window) and is now confined to status epilepticus and established regimens. The choice is usually confirmed by the neurologist, but the emergency physician must start correctly when treatment is begun in the department. [1]

Subtypes and scenarios

Alcohol-withdrawal seizure — a generalised convulsion 6 to 48 hours after cessation or reduction, typically single and self-limiting; management is benzodiazepine-based withdrawal treatment (e.g. diazepam 10 mg or lorazepam symptom-triggered), thiamine 100 mg IV before glucose, and investigation only if atypical (focal, prolonged, first, head trauma) — because the alcohol-withdrawal seizure is a diagnosis of exclusion and a subdural haematoma or a seizure from another cause is easily missed in the alcoholic. [1]

Febrile seizure (paeds) — a seizure with fever in a child aged 6 months to 5 years without CNS infection or a prior afebrile seizure; simple (generalised, under 15 minutes, no recurrence in 24 hours) is benign and needs only fever control and parental reassurance, while complex (focal, over 15 minutes, or recurrent in 24 hours) has a higher risk of later epilepsy and warrants investigation and sometimes a benzodiazepine (see the paediatric topics). [1]

Eclampsia — any seizure in a pregnant or postpartum woman is presumed eclamptic until proven otherwise and is treated first with magnesium sulfate (4 g IV over 5 to 15 minutes, then 1 g/hour infusion, or a 10 g IM loading alternative), not with the standard antiepileptic ladder; involve the obstetric team for delivery (see the hypertensive disorder of pregnancy topic). [1]

Provoked toxic seizure — tricyclic antidepressant (sodium bicarbonate 8.4 per cent 1 to 2 mmol/kg), theophylline, isoniazid (pyridoxine / vitamin B6, the antidote for the refractory seizure of INH overdose), cocaine, and withdrawal from benzodiazepines or alcohol; treat the toxin alongside the ladder. [1]

Known epilepsy with a breakthrough — check adherence and the drug level; non-compliance is the commonest cause and the easiest to fix. A first seizure over the age of 40, or in an immunocompromised patient, or with a new focal deficit, carries a high probability of a structural cause and is imaged before discharge. [1]

Complications and pitfalls

The complications of a seizure are direct and delayed. Aspiration of gastric contents (the depressed consciousness and the absent gag reflex) causes a pneumonitis and pneumonia; injury — a fall, a fracture, a shoulder dislocation, a head injury, a drown if in water; sudden unexpected death in epilepsy (SUDEP), a rare but real risk (about 1 per 1000 patient-years, higher in uncontrolled generalised tonic-clonic seizures) that the patient is counselled about — not in the emergency department at the first event, but by the neurologist at the first clinic visit. The pitfalls are the inverse of the management: missing hypoglycaemia by not checking the glucose; sending an unstable or unrecovered patient to the CT scanner; misdiagnosing a PNES or a convulsive syncope as epilepsy and committing the patient to unnecessary drugs and driving restrictions; missing a structural cause by not imaging the high-risk patient; prescribing valproate to a woman of childbearing potential; and forgetting the driving advice and the legal duty to notify the licensing authority. [1]

Prognosis and disposition

Disposition turns on the recovery and the risk. Admit the patient who has a first seizure with any of: an abnormal neurological examination or a persistent deficit, failure to return to baseline in the department, a recurrent seizure in the department, an abnormal CT, a provocative metabolic or toxic cause needing correction or observation (e.g. severe hyponatraemia, alcohol withdrawal needing a benzodiazepine regimen, drug overdose), an infectious cause needing intravenous antibiotics, poor social support or unsafe home circumstances, or a child with a complex febrile seizure or a first afebrile seizure needing workup. Discharge the recovered low-risk adult — normal glucose and electrolytes, a normal ECG, no focal deficit, recovered to baseline — with an outpatient EEG within 24 to 72 hours, an outpatient MRI arranged by the neurologist, a neurology referral, written safety advice, and the driving restriction explained and documented. The recurrence risk and the driving rules are the two pieces of information the patient must leave with. The long-term prognosis is good: most patients with a first unprovoked seizure do not develop refractory epilepsy, and immediate treatment does not change the long-term outcome — which is why counselling and a measured approach matter as much as the drug.[4][5]

Driving restrictions

Driving is the OSCE counselling question, and it is examined. The principle is a balance between the individual's mobility and the public's safety: a seizure at the wheel risks lives, so a defined seizure-free interval is required before driving resumes. The rules are jurisdiction-specific and the candidate must know the local standard. [1]

The emergency physician's job is not to grant or revoke a licence — it is to tell the patient not to drive until cleared, to explain the legal duty to notify, and to document the advice in writing in the discharge record. [1]

Special populations

The elderly present more often with a focal or a silent seizure, a prolonged post-ictal confusion (mistaken for delirium), and a structural or metabolic cause (stroke, tumour, subdural, hyponatraemia); they tolerate antiepileptics poorly (sedation, falls, interactions) and levetiracetam is preferred. The woman of childbearing potential is started on levetiracetam or lamotrigine, never valproate, with folate and contraception counselling. The pregnant or postpartum woman with a seizure is presumed to have eclampsia and is treated first with magnesium sulfate. The child with a febrile seizure follows the simple-versus-complex pathway; a first afebrile seizure is worked up and referred. The alcoholic is assessed for a withdrawal seizure (and given thiamine before glucose) but is investigated for other causes if the seizure is atypical. The known-epilepsy patient with a breakthrough is checked for adherence and the drug level before a new cause is assumed. [1]

Evidence and regional guidelines

The contemporary evidence base is the ILAE practical definition of epilepsy (Fisher 2014), which redefined a single unprovoked seizure with a high recurrence risk as epilepsy; the AAN/AES evidence-based guideline on the management of a first unprovoked seizure in adults (Krumholz 2015), which codified the imaging, EEG and counselling recommendations; the MESS trial (Marson 2005) and the Cochrane review of immediate versus deferred treatment (Leone 2021), which together established that immediate treatment delays but does not prevent long-term recurrence; and the Cochrane review of prognosis after a first unprovoked seizure (Neligan 2023), which quantified the recurrence risk and its modifiers.[1][2][3][4][5] Regional guidance is the NICE and SIGN epilepsy guidelines, the Austroads Assessing Fitness to Drive standard in Australia and New Zealand, and the DVLA At-a-Glance guide in the United Kingdom.

Landmark trials and the evidence base

The Fellowship candidate should hold the first-seizure and status-epilepticus evidence base as a small, ordered set of papers — each answers one examination question, and each is named in the OSCE and the viva. The five anchor trials are the prehospital route question (RAMPART), the second-line agent question (ESETT), the new-diagnosis drug-effectiveness question (SANAD), the recurrence-risk quantification after two seizures (Hauser), and the immediate-versus-deferred treatment question after a first seizure (MESS).[3][6][7][8][9]

Exam pearls

• Provoked versus unprovoked is the master distinction — it governs recurrence risk, antiepileptic initiation and driving. A provoked seizure is treated by removing the cause; an unprovoked seizure carries a recurrence risk of about a third at one year.
• Check the glucose first, the ECG on everyone, and image selectively — hypoglycaemia is rapidly reversible, a cardiac arrhythmia masquerades as a seizure, and a CT is not needed in the fully recovered low-risk young adult.
• A first unprovoked seizure does not automatically need an AED — MESS and Cochrane show immediate treatment delays but does not prevent long-term recurrence; treat when the recurrence risk is high (EEG, imaging, nocturnal, prior insult) or the patient chooses to after counselling.
• Levetiracetam first, valproate avoided in women of childbearing potential — broad spectrum, few interactions, teratogenicity avoided.
• Driving: 6 months off a private licence after a first unprovoked seizure, 12 months for established epilepsy, 5 to 10 years commercial; legal duty to notify.
• Not everything that shakes is a seizure — convulsive syncope recovers in under a minute with no post-ictal state; PNES has out-of-phase movements and preserved consciousness; a Todd paresis follows a witnessed convulsion and resolves.
• The first benzodiazepine is IV lorazepam 0.1 mg/kg (4 mg) or IM midazolam 10 mg if no vein — do not delay for access (RAMPART). Give a second dose at 10 minutes if ongoing, then a second-line agent; a third benzodiazepine dose adds harm without benefit.
• Buccal midazolam 0.5 mg/kg (up to 10 mg) and rectal diazepam 0.5 mg/kg are the no-access, no-IM fallbacks — buccal has largely replaced rectal in adults and older children.
• The five-bucket cause sieve — structural, metabolic, infectious, toxic/withdrawal, vascular/immune — frames every first seizure: a febrile seizure in an adult is meningitis or encephalitis until proven otherwise; a seizure with a thunderclap headache is a subarachnoid haemorrhage; an alcoholic's seizure needs a subdural excluded.
• Thiamine before or with the glucose in the alcoholic or malnourished patient — prevents precipitating Wernicke encephalopathy, but never let the hunt for thiamine delay correction of a dangerous hypoglycaemia.
• Prolactin is obsolete as a seizure marker — distinguish a seizure from its mimics with the post-ictal state, the witnessed history (tongue-bite, incontinence, cyanosis), the capillary glucose and the ECG.
• Eclampsia is treated first with magnesium sulfate, not the antiepileptic ladder (4 g IV then 1 g/h); any seizure in a pregnant or postpartum woman is eclampsia until proven otherwise.
• Document the driving advice in writing and warn the patient of the legal duty to notify — failure to notify the licensing authority invalidates insurance and carries penalties; the ED doctor advises and documents, and does not grant or revoke the licence. [1]

Red flags