Overview
Stabilise a first suspected seizure, reconstruct the event from positive clinical evidence, identify provoked and cardiac causes, and arrange timely specialist testing without using a normal EEG to dismiss epilepsy.
A seizure is a transient occurrence caused by abnormal excessive or synchronous neuronal activity. Epilepsy is an enduring tendency to recurrent unprovoked seizures and is not synonymous with a single convulsion. Acute symptomatic seizures occur in close association with an acute cerebral or systemic insult such as hypoglycaemia, major electrolyte disturbance, infection, stroke, head injury, intoxication or alcohol withdrawal. Identifying and correcting the provoking cause is urgent, but the patient may still need neurological assessment if the event or substrate creates continuing risk.
The event history should be chronological. Beforehand, ask about sleep deprivation, fever, pregnancy, medicines, missed doses, alcohol or drug use, head injury, aura, palpitations, posture, pain and emotional triggers. During the event, clarify responsiveness, eye and head position, colour, breathing, symmetry and sequence of movement, duration, vocalisation and injury. Afterwards, document confusion, sleep, headache, myalgia, weakness and time to baseline. Avoid asking only whether the person shook or was unconscious, because those labels collapse useful discriminating detail.
Aetiology
Acute provoked seizure
Hypoglycaemia, electrolyte disturbance, infection, stroke, trauma, intoxication or withdrawal can produce a time-linked seizure without establishing chronic epilepsy.
Structural cerebral disease
Previous infarction, tumour, cortical malformation, trauma or infection can create a persistent epileptogenic focus and raise recurrence risk.
Genetic or network epilepsy
A first recognised event may reveal an inherited generalised or focal epilepsy syndrome, often supported by age, semiology, EEG and family history.
Unknown cause
Some apparently unprovoked seizures remain unexplained after appropriate imaging and physiological assessment, requiring probability-based recurrence counselling.
Pathophysiology
- 1Cortical hyperexcitability
A transient insult or enduring network abnormality shifts excitation above inhibition, allowing a population of cortical neurons to discharge synchronously.
- 2Local or bilateral recruitment
Abnormal activity remains focal, impairs awareness or propagates through connected networks to produce bilateral tonic and clonic movement.
- 3Postictal suppression
After discharge terminates, inhibitory and metabolic recovery causes confusion, sleepiness, headache or transient focal weakness that resolves over time.
Clinical features and red flags
Abrupt loss of awareness followed by tonic stiffening and rhythmic bilateral clonic movements, with post-event confusion and muscle soreness, is strongly suggestive when witnessed as a coherent sequence.
A stereotyped sensory, experiential, autonomic or motor aura, unilateral onset, head version, speech arrest or postictal focal weakness suggests a seizure beginning in one cerebral network.
Prolonged standing, pain, heat, nausea, sweating, visual dimming and pallor followed by brief loss of tone, a few jerks and rapid orientation favours reflex syncope; exertional or supine collapse raises cardiac concern.
A prolonged fluctuating course, asynchronous movements, variable responsiveness or tightly closed eyes can support a functional event, but diagnosis requires positive expert assessment and no single sign is decisive.
Fever, meningism, severe metabolic disturbance, recent brain injury, stroke, intoxication or withdrawal points towards an immediate provoking process whose treatment cannot wait for an outpatient epilepsy label.
Investigations
- 01
Capillary glucose and targeted blood testsFirst step - Why
- Find reversible metabolic causes and assess consequences of a prolonged convulsion.
- Interpretation and limitations
- Correct hypoglycaemia immediately. Electrolytes, renal and liver function, calcium, full blood count, inflammatory markers, toxicology or pregnancy testing are selected from the history; non-specific postictal abnormalities require clinical context.
- 02
Twelve-lead ECG - Why
- Identify cardiac conditions that can cause transient loss of consciousness with convulsive movements.
- Interpretation and limitations
- Assess rhythm, conduction, QT interval, pre-excitation and ischaemic features. A normal resting tracing does not rule out intermittent arrhythmia, so concerning exertional, supine or family-history features require cardiac escalation.
- 03
Electroencephalography - Why
- Support a clinical epilepsy diagnosis and help classify seizure type or syndrome.
- Interpretation and limitations
- Epileptiform discharges increase recurrence probability and can guide classification. A normal routine study never excludes epilepsy; sleep-deprived or ambulatory recording may be considered when uncertainty persists.
- 04
MRI brain using an epilepsy protocol - Why
- Detect a structural substrate when epilepsy is diagnosed or a lesion is clinically suspected.
- Interpretation and limitations
- MRI is preferred for most people with diagnosed epilepsy, using regionally agreed protocols. Urgent CT is selected when an acute lesion, haemorrhage, trauma or
Differential diagnosis
Convulsive syncope
Presyncope, pallor, situational trigger and rapid recovery favour hypoperfusion; brief stiffening or jerks can occur and do not prove epilepsy.
Functional or dissociative seizure
Prolonged fluctuating movement, closed resistant eyes and variable responsiveness may support a functional event, ideally assessed through specialist semiology and video EEG.
Migraine aura or TIA
Gradually spreading positive symptoms favour aura, while abrupt negative focal loss suggests TIA; neither usually produces a stereotyped convulsion with prolonged postictal confusion.
Parasomnia or movement disorder
Events arising from sleep or recurrent dystonic, tremulous or tic-like movements require chronology, awareness and video evidence to separate them from seizures.
Management
01ImmediateStabilise and identify provocationFirst stepA person presents during or soon after a first suspected seizure.+
- 11. Protect from injury, use ABCDE, time the event, check glucose and oxygenation, and treat as status if convulsions reach five minutes or recovery fails.
- 22. Establish baseline cognition and repeat neurological examination after the postictal period, looking for trauma, meningism, pregnancy-related disease and persistent focal signs.
- 33. Obtain ECG and targeted laboratory tests, treating major metabolic, infectious, toxicological or withdrawal causes through the appropriate acute pathway.
- 44. Decide whether immediate CT, lumbar puncture, cardiac monitoring or admission is needed; do not defer dangerous-cause evaluation to the epilepsy clinic.
02ReconstructDistinguish seizure from mimicThe person is stable enough for a detailed account.+
Complications
Trauma and aspiration
Loss of awareness and motor control causes head injury, fractures, burns or drowning, while vomiting and reduced consciousness threaten the airway.
Status epilepticus
Failure of the event to stop or rapid recurrence without recovery produces cardiorespiratory, metabolic and neuronal injury requiring emergency treatment.
Recurrence and epilepsy-related death
An enduring epileptic tendency can cause further seizures, and uncontrolled tonic–clonic events contribute materially to sudden unexpected death risk.
Driving and occupational restriction
Even one seizure can temporarily prevent driving or hazardous work and create financial, safeguarding and psychological consequences while diagnosis remains uncertain.
Monitoring and follow-up
- Confirm return to neurological and cognitive baseline; persistent confusion or weakness requires reassessment for non-convulsive status, stroke, infection, injury or another acute lesion.
- Track completion and interpretation of ECG, specialist review, EEG and indicated imaging rather than assuming a referral alone closes the diagnostic loop.
- Document further events with timing, witness description, recovery and possible triggers, encouraging safe video capture only when care and privacy are not compromised.
- If medication is started, monitor seizure recurrence, adherence, adverse effects, mood, interactions and syndrome-specific laboratory or serum-level needs.
- Revisit driving, occupational and domestic safety at each diagnostic change, particularly if another event occurs or treatment is altered.
Special situations
Jerks occur in syncope
Brief myoclonic movements can accompany cerebral hypoperfusion, so the prodrome, colour, loss of tone and speed of recovery often discriminate better than shaking alone.
Tongue site adds weight
Lateral tongue trauma supports a generalised convulsion more than a non-specific tip injury, but absence of a bite cannot exclude seizure.
Postictal weakness localises
Todd paresis can persist after a focal seizure and mimic stroke; because acute stroke can itself trigger seizure, new persistent weakness still needs urgent imaging.
EEG supports a story
Interictal epileptiform activity meaningfully raises diagnostic confidence, yet incidental abnormalities and normal recordings mean EEG never replaces expert clinical history.
Provoked does not mean trivial
An acute symptomatic seizure may have a lower long-term recurrence tendency than an unprovoked event, while the underlying sepsis, metabolic failure or brain lesion may be immediately life-threatening.
Common pitfalls
- 01
Diagnosing epilepsy from one unexplained blackout without an ECG can miss an intermittent channelopathy or arrhythmia with preventable sudden-death risk.
- 02
Using urinary incontinence or a raised lactate as a stand-alone diagnostic test overstates non-specific findings that occur in several causes of collapse.
- 03
Reassuring a patient that a normal routine EEG rules out epilepsy contradicts the limited sensitivity of interictal recording.
- 04
Starting antiseizure medication before clarifying the seizure class and epilepsy type can worsen some syndromes and adds adverse effects to a possible mimic.
- 05
Discharging without driving and recurrence safety advice leaves a substantial interval of unmanaged risk before the specialist appointment.