Basic Science Physiology

Evoked Potentials

Evoked Potentials

What Do You Need to Know?

  • 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
🚩 Don’t Miss — Test-Day Priorities
  • 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 SSEPscortical (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
🔍 Buzzwords & Pathognomonic FindingsModality / wave · Anatomic generator · Clinical use
Modality / wave
  • P100 over Oz at ~100 msVEP cortical response (striate cortex/V1) — pattern-reversal checkerboard
  • 5 BAEP waves (I–V) within ~6 ms of clickbrainstem 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 stimcorticospinal tract conduction; CMCT = cortical–spinal latency
  • D-wavedirect corticospinal volley recorded epidurally during intramedullary cord tumor surgery
Anatomic generator
  • BAEP wave Idistal CN VIII (cochlear nerve)
  • BAEP wave IIproximal CN VIII (intracranial portion)
  • BAEP wave IIIcochlear nucleus (lower pons)
  • BAEP wave IVsuperior olivary complex (mid-pons)
  • BAEP wave Vlateral lemniscus / inferior colliculus (upper pons–midbrain)
  • SSEP N13dorsal column nuclei at cervicomedullary junction
  • SSEP N20contralateral primary somatosensory cortex (area 3b)
  • VEP P100primary visual cortex (V1, striate cortex)
Clinical use / disease
  • Prolonged VEP P100, clinically unaffected eyesubclinical 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-ROSChighly 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 jerkscortical (reflex) myoclonus — PMEs, Lance–Adams, JME
  • Prolonged BAEP I–III interpeak with sensorineural hearing lossvestibular schwannoma / cerebellopontine angle lesion
  • Loss of BAEP waves III–V with preserved wave Ibrainstem death pattern (classic teaching; not an accepted ancillary test under 2023 guideline)
  • > 50% amplitude drop or > 10% latency increase intraopalarm criterion — intervene (raise MAP, reposition, reverse retraction)
  • Loss of MEPs with preserved SSEPs in spine surgeryanterior spinal cord / corticospinal injury (anterior spinal artery territory)
  • Newborn click-evoked BAEPuniversal 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

AbnormalityMechanismClinical Significance
Prolonged P100 latencyDemyelination of optic nerveOptic neuritis, MS (most common cause)
Reduced P100 amplitudeAxonal loss in optic nerveCompressive optic neuropathy, severe optic neuritis, ischemic optic neuropathy
Absent P100Complete conduction failureSevere optic nerve damage, technical issue (check visual acuity)
Asymmetric half-field responsesPost-chiasmal lesionOptic 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.

Brainstem Auditory Evoked Potentials (BAEP)

Technique

  • Stimulus — monaural clicks delivered via earphones (alternating polarity); contralateral ear receives white noise masking; click stimulus 60–70 dB above threshold (sensation level) or ~70 dB nHL, presented monaurally at ~10–11 Hz
  • Recording — vertex (Cz) referenced to ipsilateral ear (A1 or A2)
  • 5 waveforms generated within 10 ms of stimulus

BAEP Waves — Generators

WaveApproximate LatencyGeneratorAnatomic Level
I~1.5 msDistal CN VIII (cochlear nerve)Inner ear / distal nerve
II~2.5 msProximal CN VIII (intracranial portion of cochlear nerve) at brainstem entry; cochlear nucleus is more associated with Wave III neighborhood. Practice pearl: Waves I, III, and V are the clinically important and most reliably identified waves; Wave II is less consistently identified and rarely used clinically.Pontomedullary junction
III~3.5 msSuperior olivary complexLower pons
IV~4.5 msLateral lemniscusUpper pons
V~5.5 msInferior colliculusMidbrain

Memory Aid: BAEP Wave Generators

  • "E-COSLIn" — Eighth nerve distal (I), proximal CN VIII / Cochlear nerve intracranial (II), Olivary complex (III), Lateral lemniscus (IV), Inferior colliculus (V)
  • Wave V is the most robust and last wave to disappear — it is the most clinically important waveform

Interpeak Latencies

Interpeak IntervalSegment TestedAbnormal In
I–IIICN VIII to lower ponsAcoustic neuroma (vestibular schwannoma), CPA tumors
III–VLower pons to midbrainMS (brainstem demyelination), brainstem stroke
I–VEntire central auditory pathwayAny brainstem lesion; prolonged in MS

Clinical Applications

  • Acoustic neuroma — prolonged I–III IPL or absent waves beyond Wave I; interaural Wave V latency difference >0.3–0.4 ms is the most sensitive BAEP criterion for vestibular schwannoma
  • MS — prolonged III–V or I–V IPL (central demyelination)
  • Intraoperative monitoring — posterior fossa surgery, CN VIII preservation
  • Brain death — absent all waves, or only Wave I present (peripheral response without brainstem conduction)
  • Infant hearing assessment — objective hearing threshold estimation in neonates (no patient cooperation needed)
Clinical Pearl

In acoustic neuroma screening, BAEP has been largely replaced by MRI with gadolinium. However, BAEP remains valuable intraoperatively to monitor CN VIII function during posterior fossa and cerebellopontine angle surgery.

Somatosensory Evoked Potentials (SSEP)

Technique

  • Stimulus — electrical stimulation of peripheral nerve (square-wave pulse at motor threshold)
  • Upper extremity — median nerve at wrist (most common)
  • Lower extremity — posterior tibial nerve at ankle (most common)
  • Pathway tested — peripheral nerve → dorsal columns → medial lemniscus → thalamus (VPL) → primary sensory cortex

Upper Extremity SSEP Waveforms (Median Nerve)

WaveformApproximate LatencyGeneratorRecording Site
N9~9 msBrachial plexus (Erb's point)Erb's point
N13~13 msCervical cord / dorsal horn (cervical spine)Posterior neck (C5 spinous process)
P14~14 msMedial lemniscus / cervicomedullary junctionScalp (far-field)
N20~20 msPrimary somatosensory cortex (contralateral)Scalp (C3' or C4')

Central conduction time (CCT) for upper extremity SSEP is typically computed as N13–N20, with P14–N20 as an alternate CCT measure.

💎 Board Pearl — SSEP Wave Memory Aid

N9 = brachial plexus → N13 = cervical cord → P14 = brainstem / medial lemniscus → N20 = cortex. Walk the signal up the dorsal column pathway and the waves localize in order. Useful for board localization questions.

💎 Board Pearl — Additional BAEP & VEP Pitfalls
  • Unilateral peripheral hearing loss: ipsilateral Wave I is absent (cochlear/CN VIII failure), but later waves (especially Wave V) can still appear via the bilateral central auditory projections — do NOT mistake preserved Wave V for intact peripheral function.
  • "No Wave I, no conclusion": if Wave I cannot be identified, the rest of the BAEP trace is uninterpretable (cannot distinguish peripheral failure from central pathology). Repeat with better technique before localizing.
  • Anoxic BAEP pattern: after severe hypoxic-ischemic injury, BAEPs typically show preserved Wave I with absent waves II–V (intact CN VIII generator, destroyed brainstem auditory pathway). Pair with bilaterally absent SSEP N20 for poor prognosis.
  • Compressive optic-pathway tumors (chiasmal meningioma, pituitary adenoma) distort the VEP waveform morphology (amplitude reduction, distortion) but typically do NOT prolong P100 latency the way demyelination does — useful imaging-vs-EP differentiator.

Lower Extremity SSEP Waveforms (Posterior Tibial Nerve)

WaveformApproximate LatencyGeneratorRecording Site
N22 (lumbar potential, ~22 ms)~22 msCauda equina / lumbar cordLumbar spine
P31~31 msSubcortical far-field (brainstem)Scalp (far-field)
N34~34 msSubcortical (brainstem/thalamic, exact generator debated)Scalp (far-field)
P37~37 msPrimary somatosensory cortexScalp (CPi or Cz')
Board Pearl

P37 is recorded paradoxically IPSILATERAL to the stimulated leg (due to medial location of foot sensory cortex on interhemispheric surface). Recording electrode typically at CPi or Cz'. Key board pearl.

Clinical Applications

  • MS — central conduction delay (prolonged N13–N20 or N22–P37 interpeak latency); subclinical spinal cord/brainstem lesions
  • Intraoperative spinal cord monitoring — monitors posterior column (dorsal column) function during scoliosis correction, spinal tumor surgery
  • Post-cardiac arrest prognostication — bilateral absent cortical N20 with preserved peripheral/cervical responses, assessed ≥48 h after ROSC = highly reliable poor-outcome predictor; use as part of multimodal neuroprognostication, not in isolation
  • Myelopathy evaluation — detect subclinical dorsal column dysfunction in cervical spondylotic myelopathy, B12 deficiency
Board Pearl

Bilateral absent cortical N20 on SSEP with preserved peripheral/cervical responses, assessed ≥48 h post-ROSC, is a highly reliable poor-outcome predictor after cardiac arrest — but it must be used as part of multimodal neuroprognostication (clinical exam, EEG, NSE, MRI), not as a stand-alone test. Avoid early/sedation-confounded conclusions.

Motor Evoked Potentials (MEP)

Technique

  • Stimulus — transcranial magnetic stimulation (TMS) or transcranial electrical stimulation (TES) over motor cortex
  • Recording — compound muscle action potential (CMAP) from target muscle (e.g., hand intrinsics, tibialis anterior)
  • Pathway tested — motor cortex → corticospinal tract → anterior horn cell → peripheral nerve → muscle

Central Motor Conduction Time (CMCT)

  • CMCT = cortical MEP latency − spinal (root) MEP latency
  • Isolates the central segment (cortex to anterior horn cell)
  • Normal CMCT — ~6–8 ms (upper extremity), ~12–16 ms (lower extremity)
  • Prolonged CMCT → corticospinal tract demyelination (MS, hereditary spastic paraplegia) or degeneration (ALS)

Clinical Applications

IndicationFindingSignificance
MSProlonged CMCTCorticospinal tract demyelination
ALSProlonged CMCT, reduced amplitude, absent responsesUpper motor neuron involvement (supports diagnosis)
Intraoperative monitoringAmplitude/latency changes during surgeryAnterior cord / corticospinal tract ischemia detection
MyelopathyProlonged CMCTCorticospinal tract compression
Clinical Pearl

Intraoperative monitoring combines SSEP (posterior columns) with MEP (corticospinal tract) to cover both the anterior and posterior spinal cord. Isolated anterior cord ischemia (e.g., anterior spinal artery syndrome) may be missed by SSEP alone — MEP provides critical complementary monitoring.

EP Comparison Table

Master Comparison of All EP Modalities

FeatureVEPBAEPSSEPMEP
StimulusPattern-reversal checkerboardMonaural clicksElectrical (median/tibial nerve)TMS or TES over motor cortex
Pathway testedOptic nerve → visual cortexCN VIII → brainstem auditory pathwayPeripheral nerve → dorsal columns → sensory cortexMotor cortex → corticospinal tract → muscle
Key waveformP100Wave V (most robust)N20 (upper) / P37 (lower)CMAP from target muscle
GeneratorStriate cortex (V1)Inferior colliculusPrimary somatosensory cortexTarget muscle (via corticospinal tract)
Most common abnormalityProlonged P100 latencyProlonged I–III or III–V IPLProlonged central conduction timeProlonged CMCT
Top clinical indicationOptic neuritis / MS detectionAcoustic neuroma, brainstem lesion (NOT brain death per 2023 guideline)Spinal cord monitoring, post-arrest prognosticationCorticospinal tract assessment, intraoperative monitoring
Sensitivity for MS85–90% (highest)~30–50% (definite MS ~50%; probable/possible MS much lower)50–70%Variable (50–70%)
EPs in Multiple Sclerosis

Sensitivity by Modality

EP ModalitySensitivity in MSWhat It Detects
VEP85–90% (with history of optic neuritis)Optic nerve demyelination (even subclinical)
SSEP50–70%Spinal cord / brainstem dorsal column demyelination
BAEP~30–50% (definite MS ~50%; probable/possible MS much lower)Brainstem auditory pathway demyelination
MEP50–70%Corticospinal tract demyelination

Role in MS Diagnosis

  • EPs detect subclinical lesions — objective evidence of demyelination in a pathway without clinical symptoms
  • VEP showing prolonged P100 in a clinically unaffected eye supports dissemination in space
  • Under the 2017 McDonald criteria, VEP is no longer required or included as supportive evidence (it was used in earlier 2001/2005 criteria). VEP remains clinically useful and the 2024 McDonald revision adds optic nerve as a topographic location with OCT/VEP support. Note: older board questions and review books may still reference VEP as evidence for dissemination in space (DIS) — that wording is based on pre-2017 criteria and is now outdated.
  • Multimodal EPs (VEP + SSEP + BAEP) increase overall sensitivity for detecting MS lesions
  • EPs are complementary to MRI — they detect functional demyelination that may not be visible on imaging
Board Pearl

VEP abnormality typically persists long-term after optic neuritis; ~10–20% normalize over years — even when visual acuity returns to normal, the P100 latency commonly remains prolonged. This makes VEP valuable for proving prior optic neuritis in a patient who now has a normal exam. VEP is the most sensitive single EP modality for MS detection.

Intraoperative Monitoring

EP Modalities for Intraoperative Use

ModalityPathway MonitoredSurgery TypeLimitations
SSEPDorsal columns (posterior cord)Scoliosis correction, spinal tumor, aortic surgeryDoes NOT monitor anterior cord (motor tracts)
MEPCorticospinal tract (anterior cord)Spinal surgery, intracranial tumor near motor cortexSensitive to anesthetic agents (especially inhalational)
BAEPCN VIII / brainstem auditory pathwayPosterior fossa surgery, CPA tumor resectionOnly monitors auditory pathway
SSEP + MEP combinedPosterior + anterior spinal cordAny spinal surgery (best practice)Most comprehensive coverage

Alarm Criteria

  • For SSEP: ≥50% amplitude drop or ≥10% latency increase → significant (alert surgeon)
  • For MEP: all-or-none / ≥50–80% amplitude drop or stimulation threshold increase ≥100 V; ⚠️ LATENCY CRITERIA DO NOT APPLY TO MEP — a common board trap; SSEP alarm rules (≥10% latency increase) are not transferable to MEP because MEP latency is highly variable shot-to-shot
  • Complete loss of waveform → critical alert (immediate surgical response)

Anesthesia & EPs

  • TIVA (propofol + ketamine or remifentanil) preferred for intraoperative monitoring
  • Volatile anesthetics (sevoflurane, desflurane, isoflurane) suppress cortical SSEP and especially MEPs
  • Subcortical SSEP components relatively resistant
  • N2O suppresses MEPs
  • Muscle relaxants abolish MEPs (avoid or use light blockade)

Alert Protocol

  • Verify technical factors (electrode displacement, anesthetic changes, blood pressure, temperature)
  • Notify surgeon immediately
  • Consider reversible causes: hypotension, hypothermia, anesthetic depth change
  • If changes persist after technical check → surgical cause likely → consider reversing recent surgical maneuver
Board Pearl

SSEP alone can miss anterior cord ischemia. The classic example is anterior spinal artery syndrome during aortic surgery — SSEPs may remain normal (dorsal columns spared) while the patient wakes with paraplegia (corticospinal tract infarcted). Adding MEP monitoring detects anterior cord compromise. Combined SSEP + MEP is the current standard of care.

Prognostication

Post-Cardiac Arrest

  • Bilateral absence of cortical N20 SSEPs with preserved peripheral/cervical responses, assessed ≥48 h after ROSC, is a highly reliable poor-outcome predictor (specific marker per ERC/ESICM 2021 and Neurocritical Care Society 2023 post-arrest neuroprognostication guidelines) — use as part of multimodal assessment, not stand-alone
  • False positive rate <1% — this is among the most specific and reliable prognostic tools after cardiac arrest
  • SSEP is relatively resistant to sedation and mild hypothermia; severe hypothermia and high-dose anesthetics can suppress cortical N20, but SSEP is generally more reliable than clinical exam or EEG in the ICU setting
  • Preserved N20 does NOT guarantee good outcome (low positive predictive value for recovery)
  • Should be interpreted in conjunction with other prognostic tools (clinical exam, EEG, NSE, brain MRI)

Brain Death

  • BAEP — absent all waves, or only Wave I present (cochlear/peripheral response without brainstem conduction)
  • Presence of Wave I with absent Waves II–V confirms absent brainstem function with intact cochlea
  • BAEP findings (absent waves II–V with Wave I preserved) support absent brainstem function but are NOT among recommended ancillary tests per the 2023 AAN/AAP/CNS/SCCM brain death/death by neurologic criteria consensus guideline. Acceptable ancillary tests are radionuclide cerebral blood-flow scan, 4-vessel catheter angiography, and TCD (adults only). EEG and evoked potentials (BAEPs, SSEPs) are no longer endorsed.

Prognostication Summary Table

Clinical ScenarioEP FindingInterpretation
Post-cardiac arrestBilateral absent N20 (SSEP)Poor prognosis (FPR <1%); most reliable single prognostic tool
Post-cardiac arrestN20 present bilaterallyDoes not guarantee good outcome (continue multimodal assessment)
Brain death (historical)BAEP: absent all waves or only Wave INOT an acceptable ancillary test per 2023 AAN/AAP/CNS/SCCM guideline; acceptable: nuclear CBF, 4-vessel angiography, TCD (adults only)
Coma (traumatic)Bilateral absent N20 (SSEP)Poor prognosis but less reliable than in anoxic injury
Clinical Pearl

SSEP-based prognostication after cardiac arrest should be performed at 24–72 hours and should not be the sole determinant. The 2023 AAN/AHA guidelines recommend a multimodal approach combining clinical exam, SSEP, EEG (absence of reactivity, status epilepticus), serum NSE levels, and brain imaging for neuroprognostication.

Quick Reference

💎 5-Minute Board Review — Evoked Potentials
TopicFact
VEPP100 latency prolonged in optic neuritis / MS (most sensitive EP for MS)
BAEPWave V is the most robust; Waves I, III, V are the clinically used waves (Wave II inconsistent)
BAEPProlonged I–III interpeak latency = acoustic neuroma (or interaural Wave V difference >0.3–0.4 ms)
SSEPBilateral absent cortical N20 with preserved peripheral/cervical responses, ≥48 h post-ROSC = highly reliable poor-outcome predictor (use as part of multimodal neuroprognostication, not stand-alone; avoid early/sedation confounds)
SSEPP37 recorded paradoxically IPSILATERAL to the stimulated leg (foot cortex on interhemispheric surface)
SSEP wave aidN9 brachial plexus → N13 cervical cord → P14 brainstem/medial lemniscus → N20 cortex
MEPMeasures corticospinal tract; latency criteria do NOT apply to MEP (all-or-none / amplitude alarms only)
Intraop monitoringSSEP monitors posterior columns; MEP monitors anterior cord (CST); BAEP for CN VIII / brainstem
AnesthesiaTIVA preferred (propofol + ketamine/remifentanil); volatile agents suppress cortical SSEP and MEP
MSVEP is the most sensitive EP modality for MS; not in 2017 McDonald criteria (older sources may still list it)
Brain deathBAEP and EEG are NOT acceptable ancillary tests per 2023 AAN/AAP/CNS/SCCM guideline (acceptable: nuclear CBF, 4-vessel angiography, TCD adults only)

Evoked Potentials at a Glance

QuestionAnswer
Most sensitive EP for MS?VEP (85–90% sensitivity)
Key VEP waveform?P100 — prolonged latency = demyelination (optic neuritis)
Most robust BAEP wave?Wave V (inferior colliculus)
BAEP in acoustic neuroma?Prolonged I–III interpeak latency
BAEP in brain death?Historically: absent all waves or only Wave I. Per 2023 AAN/AAP/CNS/SCCM consensus, BAEP is NOT an acceptable ancillary test (acceptable: nuclear CBF, 4-vessel angiography, TCD adults only).
Best prognostic test post-cardiac arrest?SSEP: bilateral absent cortical N20 with preserved peripheral/cervical responses, assessed ≥48 h post-ROSC = highly reliable poor-outcome predictor (multimodal use; not stand-alone)
SSEP pathway?Dorsal columns → medial lemniscus → thalamus → sensory cortex
MEP pathway?Motor cortex → corticospinal tract → anterior horn cell → muscle
Intraoperative alarm criteria?50% amplitude drop or 10% latency increase
SSEP alone can miss what?Anterior cord ischemia (need MEP for corticospinal tract)
What does latency reflect?Myelin integrity (prolonged = demyelination)
What does amplitude reflect?Axonal integrity (reduced = axonal loss)

BAEP Wave Generator Quick Table

WaveGeneratorQuick Memory
IDistal CN VIIIEar (cochlear nerve)
IIProximal CN VIII (intracranial)Pontomedullary junction
IIISuperior olivary complexLower pons
IVLateral lemniscusUpper pons
VInferior colliculusMidbrain (most robust)

References

  • Chiappa KH. Evoked Potentials in Clinical Medicine. 3rd ed. Lippincott-Raven; 1997.
  • Aminoff MJ. Aminoff's Electrodiagnosis in Clinical Neurology. 6th ed. Elsevier; 2012.
  • Nuwer MR. Fundamentals of evoked potentials and common clinical applications today. Electroencephalography and Clinical Neurophysiology. 1998;106(2):142–148.
  • American Clinical Neurophysiology Society (ACNS). Guideline 9D: Guidelines on short-latency somatosensory evoked potentials.
  • Wijdicks EFM et al. Practice parameter: Prediction of outcome in comatose survivors after cardiopulmonary resuscitation. Neurology. 2006;67(2):203–210.
  • Continuum (AAN). Clinical Neurophysiology and Evoked Potentials review articles.
🔒

Continue reading — sign in

The full note has more clinical pearls, tables, and board-focused tips. Free account, no fee.