Evoked Potentials

What You'll Learn

General principles — signal averaging extracts time-locked CNS responses from background noise; latency = myelin integrity, amplitude = axonal integrity
VEP — P100 waveform (striate cortex); prolonged P100 latency = optic neuritis/MS; most sensitive EP for MS
BAEP — 5 waves (CN VIII to inferior colliculus); Wave V most robust; I-III interval = acoustic neuroma. BAEPs are NO LONGER an acceptable ancillary test for brain death per 2023 AAN/AAP/CNS/SCCM guideline (acceptable: 4-vessel angiography, nuclear CBF scan, TCD adults only).
SSEP — dorsal column pathway; N20 (upper) and P37 (lower) = cortical responses; bilateral absent cortical N20 with preserved peripheral/cervical responses, assessed ≥48 h after ROSC, is a highly reliable poor-outcome predictor — use as part of multimodal neuroprognostication and avoid early/sedation-confounded conclusions
MEP — transcranial magnetic stimulation of motor cortex; CMCT = cortical latency minus spinal latency; corticospinal tract assessment
Intraoperative monitoring — SSEP for posterior columns, MEP for anterior cord, BAEP for CN VIII; alarm = 50% amplitude drop or 10% latency increase
EPs in MS — VEP most sensitive (85–90%), SSEP (50–70%), BAEP (~30–50%); detect subclinical demyelinating lesions

HighYield Pearls

VEP P100: pattern-reversal checkerboard → positive peak ~100 ms over occiput (Oz); PROLONGED P100 = optic neuritis/MS, often persists as a permanent “fingerprint” of prior demyelination even after vision recovers
BAEP wave generators (memorize): I = distal CN VIII (cochlear nerve), II = proximal CN VIII, III = cochlear nucleus (lower pons), IV = superior olivary complex, V = lateral lemniscus/inferior colliculus; I–III interpeak = lower pontine, III–V = upper pontine/midbrain
BAEP & brain death: classic teaching is loss of waves III–V with preserved wave I = brainstem death — but per the 2023 AAN/AAP/CNS/SCCM brain death guideline, BAEPs are NO LONGER an acceptable ancillary test (accepted: 4-vessel angiography, nuclear CBF, TCD in adults)
SSEP key peaks (median): Erb’s point N9 = brachial plexus, N13 = cervicomedullary junction (dorsal column nuclei), N20 = contralateral primary somatosensory cortex; tibial → N22 (lumbar) and cortical P37/P40
Bilaterally absent cortical N20 SSEP after cardiac arrest = one of the strongest predictors of poor neurologic outcome when preserved peripheral/cervical responses are present and the test is performed ≥48 h after ROSC off confounding sedation; built into post-arrest multimodal neuroprognostication guidelines — not a stand-alone test
Giant cortical SSEPs → cortical (reflex) myoclonus — progressive myoclonic epilepsies, post-anoxic Lance–Adams, JME; useful electrophysiologic biomarker of cortical hyperexcitability
Intraoperative monitoring alarm criteria: SSEP/MEP amplitude drop > 50% or latency increase > 10% triggers intervention; SSEP covers dorsal columns (posterior cord), MEP covers corticospinal/anterior cord — you need BOTH because anterior spinal artery infarcts can spare SSEPs
MEP & central motor conduction time (CMCT): transcranial magnetic/electrical stim of motor cortex → muscle response via corticospinal tract; PROLONGED CMCT in MS, ALS, cervical myelopathy, HSP
Modality-specific intraop uses: D-wave for corticospinal integrity in intramedullary spinal cord tumors, facial nerve EMG in vestibular schwannoma/parotid surgery, recurrent laryngeal (CN X) EMG in thyroid surgery, BAEP in posterior fossa/CPA surgery
Interpretation pitfalls: peripheral neuropathy delays SSEP from N9 onward (mimics central slowing — always check peripheral peaks); hypothermia/cooling prolongs all latencies; sedation & volatile anesthetics reduce cortical SSEP/MEP amplitude (TIVA preferred intraop); newborn BAEP is standard universal hearing screen

🔍 Quick ReferenceModality / wave · Anatomic generator · Clinical use

Modality / wave

P100 over Oz at ~100 ms → VEP cortical response (striate cortex/V1) — pattern-reversal checkerboard
5 BAEP waves (I–V) within ~6 ms of click → brainstem auditory pathway integrity; wave V is the most robust/last to disappear
N9 – N13 – N20 (median SSEP) → brachial plexus → cervicomedullary junction → contralateral S1 cortex
P37/P40 (tibial SSEP) → cortical response from lower-limb somatosensory cortex (paradoxical lateralization)
MEP from TMS/electrical cortical stim → corticospinal tract conduction; CMCT = cortical–spinal latency
D-wave → direct corticospinal volley recorded epidurally during intramedullary cord tumor surgery

Anatomic generator

BAEP wave I → distal CN VIII (cochlear nerve)
BAEP wave II → proximal CN VIII (intracranial portion)
BAEP wave III → cochlear nucleus (lower pons)
BAEP wave IV → superior olivary complex (mid-pons)
BAEP wave V → lateral lemniscus / inferior colliculus (upper pons–midbrain)
SSEP N13 → dorsal column nuclei at cervicomedullary junction
SSEP N20 → contralateral primary somatosensory cortex (area 3b)
VEP P100 → primary visual cortex (V1, striate cortex)

Clinical use / disease

Prolonged VEP P100, clinically unaffected eye → subclinical optic neuritis / dissemination in space in MS (most sensitive EP for MS)
Bilaterally absent cortical N20 SSEP with preserved peripheral/cervical responses, assessed ≥48 h post-ROSC → highly reliable poor-outcome predictor — used as part of multimodal coma prognostication, not as a stand-alone test (avoid early/sedation-confounded conclusions)
Giant cortical SSEPs + EEG-correlated jerks → cortical (reflex) myoclonus — PMEs, Lance–Adams, JME
Prolonged BAEP I–III interpeak with sensorineural hearing loss → vestibular schwannoma / cerebellopontine angle lesion
Loss of BAEP waves III–V with preserved wave I → brainstem death pattern (classic teaching; not an accepted ancillary test under 2023 guideline)
> 50% amplitude drop or > 10% latency increase intraop → alarm criterion — intervene (raise MAP, reposition, reverse retraction)
Loss of MEPs with preserved SSEPs in spine surgery → anterior spinal cord / corticospinal injury (anterior spinal artery territory)
Newborn click-evoked BAEP → universal newborn hearing screening
Prolonged central motor conduction time (CMCT) → MS, ALS, cervical myelopathy, hereditary spastic paraparesis

Overview

General Principles

Evoked potentials (EPs) — measure CNS conduction along specific sensory or motor pathways in response to a defined stimulus
Signal averaging — hundreds to thousands of repetitions are averaged to extract the time-locked response from random background EEG noise
Latency — reflects myelin integrity (prolonged in demyelination)
Amplitude — reflects axonal integrity and number of functioning fibers (reduced in axonal loss)
Primary clinical uses — detect subclinical lesions (especially in MS), intraoperative monitoring, prognostication
EPs test the entire pathway from stimulus to cortex — can localize lesion to peripheral, brainstem, or cortical segments

Key Terminology

Absolute latency — time from stimulus to a specific peak
Interpeak latency (IPL) — time between two peaks; localizes the segment of pathway involved
Central conduction time (CCT) — transit time through the CNS (excludes peripheral segment)
Waveforms named by polarity and latency: N = negative, P = positive, number = approximate latency in ms (e.g., N20 = negative peak at ~20 ms)

Board Pearl

Latency = myelin; amplitude = axons. Prolonged latency with preserved amplitude suggests demyelination. Reduced amplitude with normal latency suggests axonal loss or conduction block. This principle applies to all EP modalities.

Visual Evoked Potentials (VEP)

Technique and Waveforms

Stimulus — pattern-reversal checkerboard (alternating black/white squares on a screen); each eye tested separately
Recording — active electrode at Oz (occipital midline), referenced to Fz (midfrontal)
Key waveform: P100 — positive peak at ~100 ms; generated by striate cortex (V1); P100 latency 90–110 ms; interocular difference <5–10 ms is significant
Full-field stimulation — entire visual field of one eye; detects pre-chiasmal lesions (optic nerve)
Half-field stimulation — one hemifield at a time; localizes post-chiasmal lesions (optic tract, radiation)

Abnormalities

Abnormality	Mechanism	Clinical Significance
Prolonged P100 latency	Demyelination of optic nerve	Optic neuritis, MS (most common cause)
Reduced P100 amplitude	Axonal loss in optic nerve	Compressive optic neuropathy, severe optic neuritis, ischemic optic neuropathy
Absent P100	Complete conduction failure	Severe optic nerve damage, technical issue (check visual acuity)
Asymmetric half-field responses	Post-chiasmal lesion	Optic tract or radiation lesion; homonymous pattern

Board Pearl

VEP is the most sensitive EP for detecting MS. P100 latency typically persists long-term after clinical recovery from optic neuritis (~10–20% normalize over years) — it serves as a long-lasting "fingerprint" of prior demyelination. A prolonged P100 in a clinically unaffected eye supports dissemination in space.

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