Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
EEG, nerve conduction studies and electromyography
Neurology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Time-critical presentation
Urgent EEG is required when non-convulsive status epilepticus is suspected, including persistent unexplained impaired consciousness after seizures or acute brain injury. Rapidly progressive weakness with bulbar, respiratory or autonomic involvement requires immediate monitored clinical care; nerve studies must never delay ventilation, immunotherapy or specialist escalation.
Purpose and principles
Choose electroencephalography and peripheral neurophysiology for a defined clinical question, prepare patients safely and interpret sampled physiological data without treating normal or incidental findings as definitive diagnoses.
Clinical neurophysiology measures function rather than anatomy. EEG samples synchronised cortical activity over time; nerve conduction studies assess impulse propagation in accessible peripheral nerves; needle EMG assesses motor-unit and muscle electrical behaviour. These tests complement history, examination, imaging and laboratory studies. Their value rises when the request contains a precise phenotype and a decision that the result will influence.
Routine EEG usually includes awake recording and activation such as eye opening, hyperventilation or photic stimulation when safe. Epileptiform discharges can support a type of epilepsy, while focal slowing may indicate local dysfunction and generalised slowing may reflect encephalopathy. None is wholly specific. Anti-seizure medicines, sedatives, sleep, age, skull defects, metabolic illness and artefact modify the trace, so a result should be read in clinical context rather than from one automated phrase.
Peripheral studies use several variables. Latency reflects the fastest conducting fibres and distal pathway; conduction velocity assesses speed across a segment; amplitude approximates the number of functioning large sensory axons or motor units, with technical caveats; F waves and late responses sample proximal conduction. Conduction block, temporal dispersion and non-uniform slowing can support acquired demyelination, whereas uniform hereditary slowing has a different pattern.
Key points
EEG records cortical electrical potentials from scalp electrodes; it supports seizure classification, detects some electrographic seizures and evaluates encephalopathy, but it is not a brain scan and does not measure intelligence or thoughts.
A normal routine EEG does not exclude epilepsy because interictal discharges are intermittent and deep or small generators may not reach the scalp. Epilepsy remains a clinical diagnosis supported by eyewitness history and appropriate tests.
Incidental epileptiform or non-specific abnormalities do not prove that a collapse was epileptic. Interpret morphology, state, activation, medicines and pre-test probability with a clinical neurophysiologist.
Sleep-deprived, sleep, ambulatory or video EEG increases sampling or links behaviour to electrical activity for selected questions; deliberate sleep deprivation carries driving and seizure-safety implications.
Continuous EEG is used in critical care for suspected non-convulsive seizures, treatment response and some encephalopathic patterns, but artefact and sedation make specialist real-time interpretation essential.
Nerve conduction studies stimulate peripheral motor or sensory nerves and record latency, amplitude and velocity. They principally assess large myelinated fibres and may be normal in isolated small-fibre neuropathy.
Indications, selection and cautions
Interictal epileptiform activity
Spikes, sharp waves or spike–wave discharges with appropriate field and morphology can support increased seizure propensity and classification. They require expert distinction from benign variants and artefact and are not equivalent to a captured seizure.
Electrographic seizure or statusRed flag
Evolving rhythmic EEG activity in frequency, distribution or morphology can represent seizure, including without major motor signs. Critical-care patterns may lie on an ictal–interictal continuum and need urgent specialist interpretation.
Diffuse encephalopathic slowing
Generalised background slowing and reduced organisation supports diffuse cerebral dysfunction but is non-specific, occurring with metabolic, toxic, infectious, postictal and sedative states. Serial change may be more informative than one grade.
Axonal neuropathy pattern
Reduced sensory and motor response amplitudes with relatively preserved velocities in a length-dependent distribution supports axonal loss. Severe axon loss can also slow measured velocity by removing the fastest fibres.
Acquired demyelinating patternRed flag
Marked non-uniform slowing, prolonged distal and F-wave latencies, temporal dispersion or conduction block across non-compressible segments supports acquired demyelination when technical and temperature factors are excluded.
Radiculopathy on EMG
Denervation and chronic neurogenic change in muscles sharing a root but supplied by different peripheral nerves can support radiculopathy. Sensory nerve action potentials may remain normal because the lesion is proximal to the dorsal-root ganglion.
Method and interpretation
01Routine interictal EEGFirst step
Why
Support epilepsy classification and identify focal or generalised cerebral dysfunction after a clinically assessed event.
Interpretation and limitations
A normal recording does not rule out epilepsy, and an abnormal recording does not prove every event is epileptic. NICE advises using EEG to support diagnosis, not to exclude it.
02Sleep-deprived or sleep EEG
Why
Increase sampling of state-dependent epileptiform activity when routine testing is non-diagnostic and suspicion remains.
Interpretation and limitations
Sleep loss can provoke seizures and impair driving. Provide written safety instructions and use the protocol selected by the neurophysiology service rather than ad hoc deprivation.
03Ambulatory or video EEG
Why
Capture habitual episodes and correlate observable behaviour with prolonged electrical recording.
Interpretation and limitations
An event without ictal scalp change may support a non-epileptic explanation only when the habitual episode, electrode quality and seizure type make scalp EEG sufficiently sensitive.
04Motor and sensory nerve conduction studies
Why
Localise mononeuropathy and classify polyneuropathy by distribution, axonal loss and demyelinating physiology.
Interpretation and limitations
Use age-, height- and temperature-adjusted laboratory reference data. Entrapment, oedema, technical placement and coexisting neuropathy can change amplitude and latency.
Clinical next steps
01First suspected seizureHistory before interictal testingFirst stepA transient event involving loss of awareness, abnormal movement, sensory phenomena or post-event change raises possible epilepsy.+
1Obtain eyewitness and video evidence, examine, check ECG and provoking metabolic or structural factors and arrange urgent specialist assessment according to red flags and NICE timing.
2Request EEG only to support a clinically suspected epileptic event and classification; provide the event description, medicines and timing rather than asking the laboratory to 'exclude epilepsy'.
3Use MRI, sleep-deprived or ambulatory EEG and treatment decisions through the epilepsy specialist; provide seizure first aid, driving and safety advice while diagnosis remains uncertain.
02Persistent impaired consciousnessSeek non-convulsive status urgentlyA patient fails to recover after a seizure or has unexplained fluctuating unresponsiveness, subtle motor activity or gaze deviation.+
Risks, monitoring and follow-up
During prolonged EEG, time-stamp clinical events, stimulation, medicines and procedures so electrical changes can be correlated with what happened at the bedside.
After sleep deprivation, reinforce seizure, transport, work and driving precautions and ensure the patient has safe accompaniment when the service requires it.
Before needle EMG, recheck anticoagulation, bleeding disorder, lymphoedema, implanted devices and local infection because the sampled muscles may need to change.
Trend strength, reflexes, bulbar status and respiratory function clinically; neurophysiology reports are snapshots and should not determine emergency monitoring frequency.
Review final reports with the original question and communicate incidental findings or uncertainty rather than pasting technical terms without explanation.
If symptoms progress after an initially normal study, reconsider timing, anatomical coverage and alternative central or small-fibre tests with neurology or neurophysiology.
Special situations
EEG samples time
A twenty- or thirty-minute routine recording can miss intermittent discharges. Increasing recording duration or including sleep changes sensitivity, but no study substitutes for an accurate event history.
Cold limbs prolong distal latency and slow velocity, mimicking demyelination. Neurophysiology laboratories warm and measure temperature to apply appropriate reference values.
Sensory responses aid root localisation
A root lesion proximal to the dorsal-root ganglion can leave the distal sensory nerve action potential intact, whereas a distal peripheral-nerve lesion often reduces it.
EMG abnormalities take time
Spontaneous denervation potentials generally emerge after axonal degeneration reaches the muscle. Very early testing can localise conduction failure yet miss later needle changes.
Small fibres need other methods
Routine conduction studies may be normal despite painful burning and temperature loss. Specialist autonomic tests or skin biopsy are considered only after a compatible phenotype and cause assessment.
Common pitfalls
01
Requesting EEG to exclude epilepsy after a poorly described collapse.
02
Starting or stopping long-term anti-seizure treatment from one incidental EEG phrase without clinical review.
03
Delaying emergency treatment of status epilepticus while waiting for routine neurophysiology.
04
Calling every mild slowing demyelination without accounting for temperature, height and technical factors.
05
Using normal large-fibre nerve studies to deny a coherent small-fibre syndrome.
06
Ordering EMG immediately after injury and treating absent denervation as definitive exclusion.
07
Ignoring anticoagulation, lymphoedema or infection when selecting muscles for needle examination.
Practice
Two practice questions
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Question 1 of 2
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NeurologyOriginal SBA
Normal routine EEG
A patient has two well-described unprovoked Focal impaired consciousness seizures, but a twenty-minute routine EEG shows no epileptiform discharges. Which interpretation is most appropriate?
Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Needle EMG asks whether muscle is electrically active at rest and how motor units recruit with effort. Fibrillation potentials and positive sharp waves support active denervation but are not specific to root, nerve or motor-neurone disease. Large, long-duration units with reduced recruitment can reflect chronic reinnervation; short-duration small units and early recruitment can support myopathy. Sampling strategy, patient activation and the interval since injury determine sensitivity.
Demyelination tends to prolong distal latencies, slow conduction, disperse responses or cause block; axonal loss more often reduces response amplitudes. Temperature, age, height, oedema and technical factors affect values.
Needle EMG samples electrical activity within selected muscles at rest and during activation, identifying denervation, reinnervation and myopathic recruitment patterns; it does not examine every muscle or directly image a nerve root.
Denervation changes can lag an acute root or nerve injury, so test timing and muscle selection matter. A normal early study may need clinical follow-up or repeat testing.
Repetitive nerve stimulation and single-fibre EMG assess neuromuscular transmission in different ways. Abnormal jitter is sensitive but not specific and must be combined with fatigability, antibodies and the clinical syndrome.
Before testing, state symptom onset, distribution, examination, suspected level, relevant surgery or trauma, pacemaker or implanted stimulator, bleeding risk, infection risk and medicines such as anticoagulants or pyridostigmine.
Results should answer the referral question: localisation, pathophysiology, severity, chronicity and limitations. 'Abnormal neurophysiology' without clinical synthesis can misdirect care.
Neuromuscular transmission defect
A reproducible decrement on appropriate repetitive stimulation or increased single-fibre jitter supports impaired transmission. Temperature, effort, recent medicines and other neuromuscular disorders affect specificity.
05Needle electromyography
Why
Assess active denervation, chronic reinnervation, motor-unit recruitment and myopathic change in selected muscles.
Interpretation and limitations
The needle sample is invasive and anatomically limited. Timing after injury, anticoagulation, lymphoedema, infection and patient activation determine safe muscle selection and diagnostic yield.
06Repetitive stimulation and single-fibre EMG
Why
Evaluate suspected myasthenia, Lambert–Eaton syndrome and other transmission disorders when clinical and antibody data require physiological support.
Interpretation and limitations
Sensitivity depends on testing a clinically involved muscle and on temperature and medicines. Jitter can increase in denervation and myopathy, so it is not disease-specific.
07Autonomic and evoked-potential testing
Why
Assess selected autonomic pathways or central sensory conduction when specialist evaluation identifies a focused indication.
Interpretation and limitations
Protocols and normative data are laboratory-specific. These studies should answer a defined question and are not broad screening for unexplained multisystem symptoms.
1
Stabilise ABCDE, glucose and reversible metabolic causes, treat any overt recurrent seizure and obtain urgent neurological and critical-care input.
2Request emergency or continuous EEG with exact event and treatment times; do not wait for routine outpatient recording when status epilepticus is possible.
3Follow the specialist anti-seizure and sedation pathway, correlating clinical and EEG response and investigating structural, infectious, toxic and metabolic causes in parallel.
03Peripheral localisationMatch test design to anatomyFocal weakness, numbness, areflexia, fatigability or suspected root, nerve, junction or muscle disease remains after clinical examination.+
1Map onset, distribution, power, reflexes and sensory modalities and state competing localisations, functional impact and whether progression or respiratory risk requires urgent care first.
2Send a focused neurophysiology referral including side, suspected nerves or roots, timing, relevant surgery and medicines, bleeding or infection risk and the decision the result will change.
3Reconcile results with imaging and laboratory data, recognise timing and small-fibre limitations and arrange repeat or specialist testing when a coherent progressive syndrome remains unexplained.