Neurophysiological studies - electroencephalography (EEG)
What EEG records
- Records summed postsynaptic potentials of cortical pyramidal neurons (not action potentials), via scalp electrodes in the 10-20 system
- Excellent temporal resolution (milliseconds), poor spatial resolution
- The mirror image of MRI - which is why they answer different questions
- Detects only superficial cortex reliably; deep temporal, mesial frontal and deep midline activity is often invisible on a scalp EEG
Normal rhythms
| Rhythm | Frequency | Where / when |
|---|---|---|
| Alpha | 8-13 Hz | Posterior, eyes closed, awake, relaxed; attenuates on eye opening |
| Beta | >13 Hz | Frontal; *increased by benzodiazepines and barbiturates* |
| Theta | 4-7 Hz | Drowsiness, children; abnormal if prominent in an awake adult |
| Delta | <4 Hz | Deep sleep; always abnormal in an awake adult |
- Sleep: vertex waves and sleep spindles (12-14 Hz) + K complexes in N2
What EEG can and cannot do
- Can: classify a known epilepsy syndrome, diagnose non-convulsive status, characterise encephalopathy, support a diagnosis of CJD, contribute to prognosis after cardiac arrest, localise for epilepsy surgery
- Cannot: diagnose or exclude epilepsy on its own
- Sensitivity of a single routine interictal EEG in epilepsy is only ~30-50%; rises to ~80-90% with repeated and sleep-deprived recordings
- ~0.5-2% of healthy adults have epileptiform discharges - an abnormal EEG in a person without clinical events does not make epilepsy
- *Epilepsy is a clinical diagnosis. The EEG classifies it; it does not make it*
Yield
- Routine EEG is the most frequently requested neurophysiological investigation
- Yield rises with: sleep deprivation, recording during sleep, photic stimulation, hyperventilation, repeated studies, longer recording
- Non-convulsive status epilepticus found in ~8-20% of comatose ICU patients who undergo continuous EEG - and is invisible without it
- ~10-30% of "refractory epilepsy" referred for video-EEG monitoring turns out to be functional (psychogenic non-epileptic) seizures
Activation procedures
Activation procedures - and what they are for
- Hyperventilation (3 min) - provokes 3 Hz spike-wave in >90% of untreated childhood absence epilepsy; also produces benign slowing, especially in children
- Photic stimulation - photoparoxysmal response in genetic generalised epilepsies (JME ~30%, Jeavons)
- Sleep deprivation and sleep recording - activates epileptiform discharges, particularly in generalised and frontal epilepsies
Sources of error
- Artefact: eye blink, muscle, ECG, movement, electrode, 50 Hz mains
- Drugs: benzodiazepines and barbiturates -> fast beta; sedatives suppress epileptiform activity; withdrawal activates it
- Normal variants over-read as epileptiform: wicket spikes, benign epileptiform transients of sleep, rhythmic mid-temporal theta, mu rhythm, 14-and-6 positive spikes, breach rhythm over a craniotomy defect
- Over-reading a normal variant is a leading cause of the misdiagnosis of epilepsy - with years of unnecessary treatment and lost licences
- Age: EEG is markedly age-dependent; neonatal and paediatric interpretation is a separate discipline
Epileptiform patterns worth recognising
| Pattern | Syndrome |
|---|---|
| 3 Hz generalised spike-and-wave, normal background | Childhood absence epilepsy |
| 4-6 Hz generalised polyspike-and-wave + photoparoxysmal response | Juvenile myoclonic epilepsy |
| Slow (<2.5 Hz) spike-wave, abnormal background | Lennox-Gastaut |
| Hypsarrhythmia - chaotic high-amplitude disorganised | Infantile epileptic spasms (West syndrome) |
| Centrotemporal spikes, activated by sleep | Self-limited epilepsy with centrotemporal spikes (benign rolandic) |
| Focal temporal spikes/sharp waves | Temporal lobe epilepsy |
| Periodic lateralised epileptiform discharges (LPDs/PLEDs) | Acute structural lesion - HSV encephalitis, stroke, tumour; high seizure risk |
| Periodic sharp wave complexes (~1 Hz) | Creutzfeldt-Jakob disease |
| Extreme delta brush | Anti-NMDAR encephalitis |
| Triphasic waves | Metabolic encephalopathy - hepatic, uraemic, hyperammonaemic (not specific) |
| Frontal intermittent rhythmic delta (FIRDA) | Non-specific: encephalopathy, deep midline lesion |
Encephalopathy - the EEG grades severity, not cause
- Mild: slowing of the posterior dominant rhythm, excess theta
- Moderate: diffuse theta-delta, loss of reactivity
- Severe: burst suppression, then electrocerebral silence
- Wernicke encephalopathy: EEG is often normal early, with non-specific slowing of the dominant background rhythm appearing later
- So a normal EEG does not exclude it - Wernicke is a clinical diagnosis and thiamine should never wait for a test
Clinical indications
- Classify an established epilepsy and guide drug choice
- Suspected non-convulsive status - unexplained persistent confusion, coma, or failure to wake after a convulsion
- *The most under-requested urgent EEG in hospital practice*
- Suspected encephalitis - HSV (temporal LPDs), autoimmune
- First seizure - to assess recurrence risk (epileptiform discharges roughly double it, influencing whether to start treatment)
- Suspected CJD
- Prognostication after cardiac arrest - as part of multimodal assessment at >=72 h (with NSE, SSEPs, imaging, examination); burst suppression and an unreactive background are poor signs
- Video-EEG monitoring: distinguish epileptic from functional seizures; pre-surgical localisation
- Ancillary test in brain death determination where clinical testing is confounded - not a required test in the Australian standard, which is clinical or blood-flow based
Requesting properly
Reporting a request properly
- State the clinical question, the event semiology, current medications, and whether sleep deprivation is wanted
- "Rule out epilepsy" is not a clinical question and will not be answered
How an EEG result should change management
- Generalised spike-wave -> genetic generalised epilepsy -> broad-spectrum agent; avoid carbamazepine, oxcarbazepine, gabapentin, vigabatrin, phenytoin
- Focal discharges -> focal epilepsy -> sodium channel blocker (lamotrigine, levetiracetam, carbamazepine) + MRI to find a lesion
- Non-convulsive status -> IV benzodiazepine, then IV levetiracetam / valproate / phenytoin; escalate to anaesthesia in refractory cases with continuous EEG guidance
- Normal EEG with typical clinical events -> treat the patient, not the tracing
- Epileptiform EEG in someone with no clinical events -> do not treat
- Video-EEG showing functional seizures -> stop anti-seizure medication, positive explanation of the diagnosis, psychological therapy
- Delivery of this diagnosis determines outcome more than anything else that follows
Practical
- Continue anti-seizure medication before a routine EEG unless specifically instructed otherwise
- Sleep-deprived study: agreed period of restricted sleep, no caffeine on the morning
- Wash hair, no oils or product
- Advise the patient not to drive to the appointment after sleep deprivation
When to escalate from routine EEG
- Repeat with sleep deprivation if the first is normal and suspicion remains
- Ambulatory (24-72 h) EEG for frequent events
- Inpatient video-EEG telemetry for diagnostic uncertainty, functional seizure suspicion, or presurgical work-up
- Continuous EEG in ICU for refractory status, unexplained coma, and post-arrest prognostication
Associations
- Epilepsy syndromes and their syndrome-specific patterns
- Encephalopathy - hepatic, uraemic, septic, hypoxic
- Encephalitis - HSV, autoimmune (anti-NMDAR extreme delta brush)
- Creutzfeldt-Jakob disease
- Sleep disorders - polysomnography incorporates EEG
- Post-cardiac-arrest hypoxic-ischaemic brain injury
- Functional (psychogenic non-epileptic) seizures
- Drug effects - benzodiazepine and barbiturate beta, clozapine and lithium discharges
- Related neurophysiology: nerve conduction studies, EMG, somatosensory and visual evoked potentials, repetitive nerve stimulation
Change over time
- EEG abnormalities may persist after seizures are controlled - do not treat the tracing; drug decisions follow clinical seizure control
- Epileptiform activity attenuates with age in some syndromes (self-limited epilepsy with centrotemporal spikes resolves by adolescence)
- Serial EEG is useful for: monitoring non-convulsive status, post-arrest prognostication, and assessing suitability for drug withdrawal (a normal EEG before withdrawal lowers, but does not eliminate, relapse risk)
Pitfalls and harms
- Over-interpretation of normal variants -> misdiagnosis of epilepsy -> unnecessary drugs, loss of licence, loss of employment, stigma, and in women unnecessary teratogenic risk
- Under-requesting urgent EEG -> missed non-convulsive status, with deaths and prolonged ICU stays
- False reassurance from a single normal interictal study
- Delay in treating Wernicke encephalopathy while awaiting an EEG or MRI
- Skin irritation from electrodes; rare seizure provoked by hyperventilation or photic stimulation (intended, and monitored)
- The two questions an EEG answers well are "which epilepsy syndrome is this?" and "is this patient in non-convulsive status?" It answers "does this patient have epilepsy?" badly
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