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The simulator's parameter ranges, defaults and alarm rules are set to the values below. The trace physics are simplified for teaching, but the numbers and directions are drawn from these guidelines and primary sources.
| Modality | Published standard | Alarm criterion | Source |
|---|---|---|---|
| SSEP | Constant-current, PW 100–300 µs, rate 2–8/s, intensity to motor threshold; record cortical/cervical/Erb's/popliteal/T12; impedance <5 kΩ. | ≥50% amplitude drop and/or ≥10% latency increase | ACNS 11B; ASNM SEP 2024 |
| MEP | Transcranial electric; train 3–9 pulses (5–7 spine, 3–5 cranial/CoMEP), ISI 1–5 ms, 200–500 Hz; PW 50–75 µs (constant-voltage, 600V max) or 500 µs (constant-current, 200mA max); max energy 50 mJ (E=I²×PW×R). Corkscrew stimulating electrodes preferred (lower impedance, less likely to dislodge). Record muscle CMAP: monopolar-referential or bipolar, ~10 muscle channels, filter 10Hz–5kHz, sensitivity 200–500 µV, sweep 10 ms/div (100 ms total). | All-or-none CMAP loss (per protocol); graded jointly with D-wave — see alarm matrix below | ASNM MEP (Macdonald 2013); Szelényi 2007; Jahangiri FR, TCeMEP course lecture |
| EMG | Free-run (neurotonic) + triggered. Pedicle-screw: <8 mA breach concern, 10–15 explore, >15 reassuring. | Sustained neurotonic / train; low triggered threshold | Calancie 1994; ISIN/ASNM |
| EEG | 10–20 system, 16–21 ch (the simulator also offers reduced 8-, 4- and 2-channel arrays — a 2-channel bilateral montage is the minimum that still answers "is one side changing?", used where a full array will not fit the field); impedance <5 kΩ balanced; LFF 0.3–1 Hz, HFF 30–70 Hz, notch filter available; timebase 1000 ms/div (30 mm/s), display 10 s/page, sensitivity 20–100 µV/div (3 µV/mm). | Marked asymmetry: ≥50% voltage difference or ≥1 Hz frequency difference side-to-side — see EEG reading framework below | ASNM raw-EEG/qEEG; Acharya JN et al 2016; Sinha et al 2016; ASET 1998 |
| TOF | 4 supramaximal stimuli @ 2 Hz; fade >70%, T4 lost ~80%, all lost >90–95%. MEP/EMG need ≥2–4 twitches. | Guides relaxant depth (not an injury alarm) | Naguib 2017 |
| D-wave | Transcranial stim, epidural recording rostral+caudal, bipolar montage, 2 channels; filter 10Hz–3kHz, sensitivity 20 µV, sweep 2 ms/div (20 ms total); only 1–3 averages needed; peak-to-peak. | ≥50% amplitude drop (IMSCT); 30–50% decrease + muscle MEP loss → temporary deficit risk — see alarm matrix below | ASNM MEP; Medicina 2024; Shils & Deletis 2014 |
| BAEP | Monaural clicks 65–70 dB nHL, 5–12/s; Cz–A1/A2, mask non-test ear; avg 1000–2000. Waves I/III/V. | ≥1 ms wave V latency rise and/or ≥50% amplitude drop | ACNS 9C/11C; Sindou |
| VEP | Red LED flash ~1/s per eye (course-cited real-world rate: 1.1 Hz); record Oz/O1/O2 + ERG (Queen Square montage: MO/LO/RO/MF/A1-A2); ERG confirms stimulation reached the retina; avg 100–200 (ACNS clinical guideline: 100–200, up to 400 for poor waveforms). Bandpass 1–100 Hz; analysis time 250 ms. N75/P100/N135. | ≥50% N75–P100 amplitude drop; also flag extreme latency or morphology change, or a unilateral (side-to-side) difference | Kodama/Sasaki 2017; ACNS clinical guideline values (no ACNS guideline exists specifically for intraoperative VEP — applied here by analogy) |
| CCEP | Single-pulse bipolar stimulation of adjacent contacts on one cortical strip (~1 Hz, 1 ms, 5–20 mA); averaged recording from a second strip on the connected cortex. ~20–30 sweeps, recording time 1–2 min per connection. | ≥50% N1 amplitude decline vs baseline; some series warn from >15% | Yamao 2017; Mariani 2021; Giampiccolo 2021; Seidel 2024 |
| CAP / NAP | Bipolar hook or tripolar electrodes directly on the exposed nerve; stimulate proximal, record distal across the lesion. Short interelectrode distances, so alternating stimulus polarity is used to cancel artifact. Few sweeps needed — the signal is large. | PRESENCE or ABSENCE across the lesion is the finding, not the number — present → neurolysis, absent → resect and graft | Kline 1993; Robert 2009; Oberle 1997; Gutiérrez 2021 |
VEP physiologic confounders modeled/cited in this simulator: temperature (~15% central-conduction slowing per 1°C drop → P100 latency shift), MAP/hypotension and blood loss (amplitude ↓, latency ↑), and anesthetic depth (sevoflurane markedly suppresses flash VEP amplitude/latency in a concentration-dependent way; propofol/TIVA far less so — Masui 2006;55:692-8; Watson & Shah 2000). Alarm troubleshooting order modeled here follows the taught sequence: check anesthetic/physiologic values → check ERG (rules out a stimulus-delivery problem) → check goggles (rules out a mechanical fault) — before calling a true surgical change. VEP's intraoperative efficacy is genuinely debated in the literature (Harding 1990; Goto 2007; Chung 2012; Kodama 2010; Neuloh 2010) — the simulator's clean alarm thresholds are a teaching simplification, not a claim of clinical consensus.
Sources for the CCEP, CAP and anaesthesia sections above (cited by author, journal and year rather than linked, so the citation can be checked without relying on a link that may rot):
CCEP — Yamao et al., Human Brain Mapping 2017 (the 50% N1 cut-off); Mariani et al., World Neurosurgery 2021 (the >15% warning threshold); Giampiccolo et al., Clinical Neurophysiology 2021 (P1/N1 latencies, directional asymmetry); Seidel et al., Clinical Neurophysiology 2024 (awake vs asleep comparison); Titov et al., Neurosurgical Review 2022 (systematic review and meta-analysis); Matsumoto et al. 2004 (original description).
CAP / NAP — Kline et al., Canadian Journal of Neurological Sciences 1993 (25-year series); Robert et al., Neurosurgery 2009 (1736 patients, technical pitfalls); Oberle et al., Neurosurgery 1997; Kim et al., Neurosurgery 2004 (318 peroneal lesions); Zelenski et al., Journal of Hand Surgery 2023 (review); Wu et al., J Clin Monit Comput 2020 (alternating-polarity artifact reduction).
Ketamine — Andleeb et al., Asian Spine Journal 2021 (randomised, 0.5 mg/kg/h); Schubert et al., Anesthesiology 1990 (cortical vs noncortical SSEP); Masapu et al., J Neuroanaesthesiol Crit Care 2026 (scoping review, dose dependence); Sloan, J Clin Neurophysiol 1998 (agent review); Akeju et al., Clinical Neurophysiology 2016 (gamma-burst EEG); Blain-Moraes et al., Frontiers in Systems Neuroscience 2014 (absence of frontal alpha); Ma et al., Anesthesia & Analgesia 2025 (adjunct agents scoping review).
SSEP fibers are heavily myelinated, large-diameter dorsal-column fibers conducting ~58 m/s. Each obligate peak has a fixed generator and vascular supply, so the pattern of which peaks change localises the problem. The peripheral responses (N9 Erb's, N11 popliteal fossa) prove stimulator integrity and are the first thing to check when a cortical drops.
| UE peak | Montage | Generator | Artery | Field / type |
|---|---|---|---|---|
| N9 (Erb's) | EPc–EPi | Brachial plexus / ascending fibers | Subclavian | Near-field, propagated — proves stim integrity |
| N13 (cervical) | EPc–C5S | Postsynaptic cervical cord (dorsal horn) | Posterior spinal | Near-field, stationary |
| P14 | EPc–CPi | Caudal medial lemniscus (lower brainstem) | Basilar | Far-field |
| N18 | EPc–CPi | Rostral brainstem / thalamus | Basilar | Far-field |
| N20 / P23 | CPi–CPc | Contralateral postcentral gyrus (primary sensory cortex) | Middle cerebral | Near-field, cortical |
| LE peak | Montage | Generator | Artery | Field / type |
|---|---|---|---|---|
| N11 (popliteal fossa) | PFp–PFd | Ascending fibers through popliteal fossa | Femoral | Near-field, propagated — proves stim integrity |
| LP (lumbar potential) | IC–T12 | Postsynaptic lumbar dorsal cord | Adamkiewicz / posterior spinal | Near-field, stationary (analogous to UE N13) |
| P31 / N34 | C5S–FPz | Caudal / rostral brainstem | Vertebrobasilar | Far-field (analogous to UE P14/N18) |
| P37 / N45 | FPz–CPz / CPc–CPi | Postcentral gyrus (medial leg area) | Anterior cerebral | Near-field, cortical |
Stationary responses (N13, LP) hold the same latency wherever the electrode sits along the segment (only amplitude varies); propagated responses (N9, N11) shift latency with limb length. The LP is the lumbar spinal peak (~N20–N22 latency) — not the cortical N20. Nerve selection by level (ACNS 11B): above C6 → median; lower cervical (above C8) → ulnar; below C8 → posterior tibial or common peroneal. UE nerve choice: median (mixed, most reliable, highest amplitude) > ulnar (mixed, good for C8/T1, medium) > superficial radial (pure sensory, supplemental, lowest, no twitch).
Alarm threshold (the "50/10 rule"): a ≥50% amplitude drop and/or ≥10% latency prolongation from baseline is reported immediately to surgeon and anaesthesia. History: Nash (1977) called a 50% amplitude drop a change; Nuwer & Dawson (1984) validated it on the P37; ACNS 11B (2009) codified 50%/10%. Two criteria for abnormality: (1) absence of an obligate waveform that had reproduced, and (2) interpeak-latency prolongation, which localises the lesion:
| Interpeak | Segment monitored |
|---|---|
| UE N9–N13 | Plexus → cervical cord |
| UE N9–P14 | Plexus → lower brainstem |
| UE P14–N20 | Lower brainstem → sensory cortex |
| UE N9–N20 | Whole pathway (periphery → cortex) |
| LE LP–P31 | Lumbar cord → brainstem |
| LE P31–P37 | Brainstem → sensory cortex |
| LE LP–P37 | Whole pathway |
Preserved SSEPs do not guarantee motor preservation — SSEP watches the dorsal columns, MEP the ventral cord; post-op paraplegia with unchanged SSEPs is documented, so pair the two. Baseline risk context (11B): scoliosis instrumentation 0.5–1.6%; cord-tumour / trauma decompression ~20%; descending thoracic aortic surgery up to ~40% paraplegia.
When a cortical response drops, work the change in a fixed order. First check the peripheral response (N9 Erb's, N11 popliteal fossa):
| Peripheral response | Points toward | Next step |
|---|---|---|
| PRESENT (peripheral intact, cortical lost) | Central cause | Surgical / perfusion (focal, side-locked) vs. anaesthetic / physiologic (global, symmetric) |
| ABSENT (peripheral also lost on that limb) | Peripheral / technical / positional | Stimulation, hook-up, or a positional plexopathy on that limb |
Visualise & articulate — state the side (L / R / bilateral), which derivations, the % change, and whether amplitude and/or latency; then walk the differential: Technical (hook-up, stim / recording parameters, electrodes, machine); Positional (BP cuff on the monitored arm, Mayo stand / chest piece leaning on the patient, shoulder taping, arms pulled down for X-ray, cold extremity, C-arm); Anaesthetic (bolus vs. continuous infusion, agent / MAC change); Physiologic (MAP, temperature, HCT / blood loss, perfusion). A benign positional or BP-cuff change resolves when the cause is removed — alerting the surgeon for it is a false alarm.
| Parameter | Value / effect |
|---|---|
| Stimulus | Monophasic rectangular; PW 100–300 µs; intensity 2.5–3× motor threshold (11B: 30–40 mA); constant-current preferred for OR (~1:4 V:mA); stimulate unilaterally for specificity |
| Stim rate | 3–7 Hz, not divisible by 60 (avoid line-locked artifact); 11B 2–8 Hz; rates >15 Hz can abolish LE-SSEP corticals (P37 ↓ up to ~80%); UE tolerates up to ~31 Hz |
| Bandpass | 30–3000 Hz (11B 30–1000 Hz). Excessive LFF → phase lead (peak earlier, falsely shorter latency); excessive HFF → phase lag (peak later, falsely longer latency) |
| Averaging | 500–2000 sweeps (far fewer in OR, ~200 once SNR allows); two trials must reproduce; artifact-reject 10–30% optimal |
| Analysis window | ≥2× the last obligate latency (UE ~40 ms, LE ~60 ms) |
| Impedance / amp | <5 kΩ; <3 kΩ inter-electrode; amplifier CMRR ≥80 dB (10,000:1) |
Stim-artifact fixes, in order: check stim impedance → re-prep skin → lower intensity → reposition closer to the nerve → use a stimulus delay / blanking window (careful not to blank real peaks) → check the ground and move it between the stimulator and the first recording site. Physiologic thresholds: keep MAP within 10–20% of the patient's baseline; SSEP deteriorates at ~18 °C core (hypothermia) and is affected at ~41 °C (hyperthermia); a cold extremity / IV / irrigation slows peripheral conduction; watch hypoxia and blood loss (H&H). Anaesthesia: steady state, ≤1 MAC halogenated with no / minimal N₂O, continuous infusion rather than boluses. Specialised SSEP: saphenous-nerve SSEP monitors the femoral nerve / upper lumbar roots in XLIF/DLIF (distal stim > proximal; CPz–CPc and CPz–Fz derivations); SSEP collision monitoring validates spinal-cord-stimulator placement (the antidromic SCS volley collides with the orthodromic SSEP, diminishing the baseline).
| D-wave | Muscle (CMAP) response | Predicted motor status |
|---|---|---|
| Unchanged | Preserved | Unchanged |
| Unchanged | Lost (one or both sides) | Temporary motor deficit |
| 30–50% decrease | Preserved | Unchanged |
| 30–50% decrease | Lost (one or both sides) | Temporary motor deficit |
| >50% decrease | Lost | Long-term motor deficit |
This matrix is the real basis for grading a combined D-wave + muscle-MEP change rather than treating either as a standalone on/off alarm — a preserved D-wave with lost muscle responses still predicts only a temporary deficit, while a D-wave drop >50% with lost muscle responses predicts a long-term one. Historically, motor function was checked with the Stagnara wake-up test (waking the patient intraoperatively to ask them to move) — it works but can usually only be done once, so the injury-to-detection interval can be large, and it's not usable in patients who can't follow commands (e.g., deafness, cerebral palsy); continuous TCeMEP/D-wave monitoring is preferred for exactly this reason.
MEP safety notes: there are no true contraindications, but extra caution/consent discussion applies for children under 2, a seizure history, pacemakers, cochlear implants, and deep brain stimulators. TOF for relaxant-depth monitoring should be recorded from distal/foot muscles, never the face or hand, during spine surgery. MAC (anesthetic potency) is decreased by increasing age, hypothermia, and pregnancy, and increased by hyperthermia — duration of anesthesia and sex have no effect. Preferred TIVA dosing: propofol 100–200 µg/kg/min with fentanyl 0.05–0.3 µg/kg/min (or remifentanil 0.5–2 µg/kg/min), no volatile agent, no muscle relaxant after induction, TOF 4/4. Mechanistically, inhalational agents suppress MEPs because they inhibit the interneuron generators that produce I-waves at the cortical level and anterior horn cell — this is why even low-dose volatile use degrades TCeMEP more than SSEP/EEG.
Double-train stimulation (a technique not modeled in this simulator's trace physics, documented here for reference): two trains of 3–9 pulses fired with an inter-train interval (ITI) of 15–150 ms, on top of the usual 1–5 ms inter-stimulus interval (ISI). Too-short an ISI falls in the refractory period; too-long an ISI gives insufficient temporal summation. A shorter ISI tends to improve upper-limb MEP, a longer ISI tends to improve lower-limb MEP. Real documented case: a 19-year-old female scoliosis-correction patient, intact pre-operatively, had unilateral (left) lower-extremity TCeMEP loss and subsequent recovery (quadriceps/tibialis anterior channels) — the same loss-then-recovery pattern modeled in this simulator's "Scoliosis correction" case (Jahangiri et al. 2014).
Triggered EMG tests screw placement electrically. A screw seated in intact cortical pedicle bone (an insulator) needs a high stimulus to reach a nerve; a pedicle-wall breach lets current out, so a nerve fires at a low threshold. Stimulate the screw (cathode on the screw, anode in proximal paraspinal muscle); constant-current is less variable than constant-voltage (Maguire 1995, Toleikis 2002). Thresholds are guidance, not absolutes, and are always used alongside palpation and radiography.
| Level | Reassuring | Explore / caution | Breach / neural contact | Source |
|---|---|---|---|---|
| Lumbar | >8 mA | 4–8 mA (possible pedicle crack) | 0–3 mA (probable neural contact); <10 mA concerning | Calancie 1994; Glassman 1995; Lenke 1995; Clements 1996 |
| Cervical | >15 mA | 10–15 mA (exploration) | <10 mA (explore, reposition, possible removal) | Djurasovic 2005 (150 µs, 5 Hz, TOF 4/4) |
| Thoracic | Reliable only T10–T12 (<6 mA = breach) | T2–T9 unreliable — lean on TCeMEP / SSEP | Medial breach → cord; lateral breach → aorta / vessel | Raynor 2001; Kuklo 2002; Samdani 2011 |
Stim-current ceilings (so current does not spread to adjacent levels): direct nerve ≤2–3 mA, pedicle ≤20 mA, pin/screw ≤30 mA. Normal direct nerve-root baseline is 1.2–3.8 mA (Calancie / Maguire). Recording: bandpass 10–3000 Hz, sensitivity >100 µV, analysis 100 ms/div for t-EMG (2000–5000 ms/div for free-run). t-EMG gives instantaneous single-root feedback — its edge over SSEP, which monitors the dorsal cord across multiple levels and can miss a single malpositioned screw (Gundanna 2003).
| Pattern | Character | Significance | Report? |
|---|---|---|---|
| Burst | Short, non-repetitive, asynchronous | Usually manipulation / decompression; rarely injury | Report if during screw placement or if frequent |
| Train | Long, repetitive, synchronous (can last minutes) | Nerve stretch / compression; may be injury | ALWAYS report |
Report the waveform and muscle, not the root — "EMG firing in the left tibialis anterior," never "the L4 root is firing." Artifact discrimination: asynchronous activity across most channels with a dry / cold field = the patient getting light → tell anaesthesia; synchronous spikes on all channels at once = metal-on-metal artifact. Subdermal needle pairs (not surface electrodes) are required to detect neurotonic discharges (Skinner 2008); use bipolar derivations and do not reference one muscle group against another.
| Direction | Causes | Fix / caution |
|---|---|---|
| Falsely LOW (over-alarming) | Osteoporosis, age, smoker, chemotherapy, soft / porous low-density bone; bicortical S1 screws near the lumbosacral plexus; S1 thin cortex | Correlate with history; expect naturally lower thresholds at S1 |
| Falsely HIGH (false-negative — dangerous) | Chronically compressed / injured root may not fire (Szkiladz 1995); fluid / blood / soft-tissue shunting; bone wax and hemostatic resistance; polyaxial screw crown absorbs energy; HA-coated / porous / 3D-printed screws insulate | Suction the wound before stimulating; stim the screw shaft / hex port, not the mobile crown (Wierzbowski 2008); for coated screws, stim the tapped pedicle with a probe |
Aggregate / outlier method: compare every screw to the others — one screw reading 12 mA when the rest read 26–30 mA warrants a second look even though 12 mA is nominally "safe." If no screw yields a CMAP at all, test a nerve root to confirm system integrity, check for fluid or bone wax, and look for stim artifact and a paraspinal twitch before calling the screws well-placed.
EMG and MEP need functioning neuromuscular junctions, so residual paralytic is the most common reason they look absent. Non-depolarizing agents compete at the ACh receptor and produce TOF fade; the depolarizing agent succinylcholine reduces twitch amplitude without fade (and can trigger malignant hyperthermia).
| Agent | Type | Approx. duration |
|---|---|---|
| Succinylcholine | Depolarizing | 5–10 min (fasciculations; good for intubation / positioning baselines) |
| Rocuronium | Non-depolarizing | 30–60 min (sugammadex-reversible) |
| Vecuronium | Non-depolarizing | 30–60 min |
| Pancuronium | Non-depolarizing | 60–90 min |
| TOF count | Receptors blocked |
|---|---|
| 1 | >95% |
| 2 | 85–90% |
| 3 | 80–85% |
| 4 | 70–75% |
Viability for t-EMG / MEP: T1b at 5–50% of the T1 baseline, or T4:T1 ≥0.75 (≤25% fade); Minahan 20/100 = 0.2 is acceptable for motor testing. Reversal: acetylcholinesterase inhibitors (neostigmine — needs ≥1 twitch present) vs. sugammadex (binds rocuronium / vecuronium directly, no twitch required). Do not rely solely on anaesthesia's TOF — watch for visible twitches during SSEP stimulation, and allow ≥10 s between TOF tests for recovery.
| Region | Level → muscle |
|---|---|
| Cervical | C2–4 trapezius · C5–6 deltoid / biceps · C6–7 flexor carpi radialis · C6–8 triceps / flexor carpi ulnaris · C8–T1 abductor pollicis brevis / abductor digiti minimi (hand) |
| Thoracic | T2–5 intercostals · T5–8 rectus abdominis (upper / mid) · T9–11 rectus abdominis (lower) · T12 external oblique · L1 internal oblique / iliopsoas |
| Lumbosacral | L2–4 adductor longus / vastus · L4–5 tibialis anterior (foot drop) · L5–S1 peroneus longus · L5–S1–S2 biceps femoris · S1–2 medial gastrocnemius · S1–2 abductor hallucis |
Subdermal needle pairs, bipolar; peroneus longus can double as peroneal-nerve SSEP stimulation. Choose channels from the roots at risk for the planned levels.
Read every IONM EEG in the same order to build a consistent, reproducible description: Patient state → Montage (filters/settings, sensitivity/timebase) → Continuity → Symmetry (voltage, then frequency) → Abnormalities. Symmetry cannot be assessed on a limited/incomplete montage or without measuring — improperly placed electrodes change inter-electrode distance, which changes amplitude.
| Continuity | % periods of suppression/attenuation |
|---|---|
| Continuous | <1% |
| Nearly continuous | 1–9% |
| Discontinuous | 10–49% |
| Burst-suppression | 50–99% |
| Suppression | >99% |
Within a burst-suppression pattern: suppression = inter-burst activity <10 µV; attenuation = inter-burst activity >10 µV but <50% of burst amplitude. A "burst" itself is ≥0.5s and ≤30s with at least 4 phases.
| Voltage (amplitude) | Range |
|---|---|
| Suppressed | <10 µV |
| Very low / low | 10–49 µV |
| Normal | 50–149 µV |
| High | ≥150 µV |
| Frequency band | Range | Typical amplitude | Source |
|---|---|---|---|
| Beta | ≥13 Hz | Low (<20 µV) | Anesthetic agents |
| Alpha | >8–<13 Hz | Low–moderate (20–150 µV) | Physiologic / anesthetic |
| Theta | >4–<8 Hz | Low–moderate (20–150 µV) | Physiologic / anesthetic |
| Delta | >1–<4 Hz | High (>150 µV) | Structural lesion / anesthesia |
| Symmetry | Voltage difference | Frequency difference |
|---|---|---|
| Symmetric | Minimal | <0.5 Hz |
| Mild asymmetry | <50% | 0.5–1 Hz |
| Marked asymmetry | ≥50% | ≥1 Hz |
Montage tradeoff: Referential localizes via maximal amplitude but is vulnerable to a polluted reference and variable inter-electrode distance. Bipolar localizes via phase reversal and makes symmetry assessment easier, but is subject to end-of-chain phenomena. IONM typically uses an A-P (longitudinal) bipolar montage, often modified around the surgical field (e.g., a channel shifted posterior/lateral to accommodate access). This simulator lets you switch montage type (bipolar / referential) and channel array (4-ch reduced, 8-ch double banana, 16-ch full 10–20) from the EEG settings; the window title, electrode count and the live read (predominant frequency · continuity · symmetry) update to match. Remember the ACNS caveat: a reduced/limited montage cannot reliably establish symmetry, so the 4-ch array is deliberately teaching-limited.
BAEPs track auditory transmission from the cochlea through the brainstem to the midbrain. Because every generator is subcortical, BAEPs are highly resistant to anaesthesia (a major advantage) though latency is prolonged by hypothermia. Analyse waves I, III and V — waves II and IV are inconsistent even in normal subjects. Wave V is the largest, most robust, and the last to disappear. Chiefly used in cerebellopontine-angle and skull-base surgery (vestibular schwannoma, microvascular decompression), posterior fossa and brainstem cases, for hearing preservation.
| Wave | Generator |
|---|---|
| I | Distal cochlear nerve (CN VIII, extracranial) |
| II | Proximal CN VIII / cochlear nucleus (upper medulla) |
| III | Superior olivary complex (lower pons) |
| IV | Lateral lemniscus (upper pons) |
| V | Inferior colliculus (midbrain) |
Localisation by interpeak latency (I–III = periphery → lower pons, III–V = lower pons → midbrain, I–V = whole brainstem transmission ~4 ms): loss or delay of wave I = cochlear / distal CN VIII ischaemia (AICA / internal auditory artery territory); wave I preserved but III/V lost = proximal CN VIII or lower pons; I and III preserved but V lost = brainstem between lower pons and midbrain.
Stimulus: monaural rarefaction / alternating clicks 65–70 dB nHL, rate ~11/s (avoid multiples of line frequency), with contralateral white-noise masking; record Cz–A1/A2 (ipsilateral ear or mastoid); average 1000–2000; bandpass ~150–3000 Hz; 10–15 ms window. Alarm (ACNS 11C): wave V latency increase ≥1.0 ms (or ≥10%) and/or amplitude drop ≥50%. A creeping wave V latency during retraction or drilling warns of CN VIII stretch or heating; an abrupt loss suggests AICA ischaemia.
Wave III is the single most sensitive predictor of post-operative hearing loss (Matthies & Samii 1997) — in a retrocochlear pattern (retraction, tumour–nerve dissection, drilling) waves I and II stay put while wave III falls first and V follows, so watch III closely. Contrast the peripheral / cochlear pattern (AICA / internal-auditory-artery ischaemia), where wave I collapses and everything downstream goes with it. Alarm nuance (ASNM AEP position statement): the classic 50%-amplitude / 10%-latency criterion has not been proven predictive of post-op hearing, and subtle changes have still produced deficits — so report any change beyond expected variability that anaesthesia or technical factors cannot account for, rather than waiting for a fixed threshold.
VEPs monitor the visual pathway from retina → optic nerve → chiasm → optic tract → lateral geniculate → optic radiations → occipital striate cortex, where the P100 arises. Used near the optic apparatus: pituitary / sellar (transsphenoidal), craniopharyngioma, tuberculum sellae meningioma, and optic-nerve / orbital surgery. Only flash stimulation (LED goggles) works under general anaesthesia — pattern-reversal is not feasible in the anaesthetised eye.
| Component | Mean latency | Note |
|---|---|---|
| N75 | ~77 ms | First negative peak |
| P100 | ~98 ms | Key positive peak; amplitude measured N75→P100 peak-to-peak |
| N135 | ~122 ms | Later negative peak |
Alarm: a >50% fall in the N75–P100 peak-to-peak amplitude versus control — after excluding a false positive — warns the surgeon. Reliable flash VEP needs three things together (Kodama / Sasaki 2017): TIVA with propofol titrated by BIS (propofol suppresses the VEP at high dose; volatile agents far more so), a high-intensity LED flash device, and simultaneous ERG to confirm the flash reached the retina. Confounders: anaesthetic depth, temperature, hypotension / blood loss, pupil size and globe compression. Troubleshooting order: check anaesthetic / physiologic values → check the ERG (rules out a stimulus-delivery problem) → check the goggles (mechanical fault) → only then call a true surgical change. Intraoperative VEP remains debated: historically unreliable owing to anaesthetic sensitivity and variability, with TIVA + ERG improving reproducibility but efficacy not universally accepted.
A single electrical pulse delivered to one patch of cortex produces a response in the cortex it is connected to. Stimulate through a strip over the anterior (Broca) language area, record from a strip over the posterior (Wernicke) area, and the response is carried by the arcuate fasciculus — the dorsal language pathway. CCEP therefore monitors a network, not a point, which is what direct cortical stimulation mapping cannot do.
Its decisive advantage: it works under general anaesthesia and needs no cooperation from the patient. Awake craniotomy is the gold standard for language mapping, but many patients cannot have one — children, the anxious, the cognitively impaired, airway or positioning problems. CCEP gives those patients language-pathway monitoring anyway. Recording one connection takes 1–2 minutes and is highly reproducible.
| Component | Typical latency | Meaning |
|---|---|---|
| P1 | ~12 ms | First positive deflection |
| N1 | ~21 ms | The monitored component. Reflects the direct cortico-cortical pathway; its amplitude is the marker of tract integrity |
| N2 | ~50–250 ms | Later, broader, more anaesthesia-sensitive; not the alarm component |
Alarm: Yamao (2017) proposed a 50% N1 amplitude decline as the cut-off to prevent permanent language dysfunction — the same figure used for MEP. Mariani (2021) was more conservative: no patient with a 0–15% decline had a deficit, while declines of 24% and 28% both produced transient postoperative speech disturbance, so that series suggests warning above 15%. A meta-analysis (Titov 2022) found a strong correlation between N1 decline and the severity of postoperative speech deficit.
Direction is not symmetric. The best response may come from stimulating anterior and recording posterior, or the reverse, and it varies between patients — establish which direction gives the stable, reproducible response at baseline and monitor that one. Giampiccolo (2021) evoked responses only when stimulating frontal and recording temporal, with none in the reverse direction. In the simulator: switching the stim→record direction to Temporal → Frontal drops the response markedly, and CCEP holds up under volatile agent while MEP collapses — set 1.0 MAC and compare the two windows.
Recorded directly from a surgically exposed nerve, this is the decision-making tool of peripheral nerve surgery. The problem it solves: a nerve injured but still in continuity looks the same to the eye whether it is regenerating or scarred through. Visual inspection is misleading, and EMG in the early months cannot settle it either. Resecting a nerve that was recovering does the patient real harm; leaving one that never will, wastes the window for repair.
The rule: stimulate proximal to the lesion and record distal to it. A NAP recorded across the lesion means axons have grown through — perform neurolysis only. No NAP means a neurotmetic lesion — resect it and graft. Kline's 25-year series: neurolysis on a recordable NAP gave good function in 93%; absence of a NAP was, without exception, neurotmetic. Robert (2009), 1736 patients and 3459 lesions: 94.7% reached grade 3 or better. Where only part of the cross-section responds, a split repair grafts the silent fascicles and spares the conducting ones.
Presence or absence is the finding — far more than latency, amplitude or shape. The threshold is physical: roughly 4000–5000 intact or regenerating axons are needed before any NAP can be recorded at all, which is why the answer is binary rather than a gentle fade. Critically, neuromuscular block does NOT abolish a NAP — you are recording from nerve, not muscle. That is the key contrast with MEP and EMG, and it means a paralysed patient can still be assessed this way.
Pitfalls: stimulus artifact is the main enemy, because the stimulating and recording electrodes are necessarily close together — alternating stimulus polarity cancels it. Also: volume conduction from a neighbouring nerve (a response that is not from the nerve you think), a cold field, tourniquet use, and local anaesthetic in the field. In the simulator: switch the recording site between across / proximal / distal, and set stim polarity to Fixed to see the artifact swamp the trace.
Order of sensitivity, most suppressed first: MEP ≈ VEP > cortical SSEP > EEG > BAEP ≈ D-wave. Halogenated agents cause dose-related amplitude loss and latency increase, worst in cortically generated responses; subcortical, spinal and peripheral responses are far more robust. This is why a monitored case runs on TIVA. Opioids largely spare evoked potentials. Neuromuscular block abolishes muscle responses (MEP, EMG) but leaves sensory and nerve recordings alone.
| Agent | Effect on IONM | Practical note |
|---|---|---|
| Halogenated volatiles | Dose-related suppression; MEP/VEP worst | Keep ≤0.5 MAC if used at all with MEP; ideally none |
| Propofol | Dose-related suppression, milder than volatiles | The backbone of a monitoring TIVA; produces the frontal alpha on EEG |
| Opioids | Minimal | Carry the anaesthetic so propofol can stay down |
| Neuromuscular blockers | Abolish MEP/EMG; no effect on SSEP, BAEP, D-wave, CAP | Watch the TOF — MEP/EMG need ≥2–4 twitches |
| Ketamine | Augments — the exception | See below |
| Etomidate | Augments cortical SSEP amplitude | Same direction as ketamine; limited by adrenal suppression |
Ketamine is the one agent that makes evoked potentials bigger, which is why it is used as an adjunct to spare propofol in a monitoring TIVA. At around 0.5 mg/kg/h it augments MEP amplitude — a randomised trial (Andleeb 2021) recorded gains of 24–100% over baseline, building over 30–60 minutes, with no latency change. Schubert (1990) showed it increases the cortical SSEP amplitude while noncortical amplitude and every latency stay unchanged, so the cortical peak grows away from an unaltered Erb/N13/popliteal response.
The dose response is not linear. A scoping review of 13 studies (Masapu 2026) found 7 showing increased MEP amplitude, 4 no change, and 2 transient suppression — and the suppression cases were high bolus doses, while low-dose or infusion regimens consistently augmented. On EEG ketamine does not look like propofol: Akeju (2016) described a "gamma burst" pattern of alternating slow-delta and gamma with increased theta and decreased alpha/beta, and Blain-Moraes (2014) showed it specifically fails to produce propofol's frontal alpha — so processed depth indices can read misleadingly light. Being sympathomimetic it also raises MAP and heart rate, which supports the signals in its own right. In the simulator: the Ketamine slider is in Patient ▸ Anaesthesia — push it past 0.8 mg/kg/h to watch the augmentation reverse.
Sources: ACNS 11B · ASNM SEP 2024 · ASNM MEP · Szelényi 2007 · ASNM EEG · Naguib 2017 · Medicina 2024 · ACNS 9C · Flash VEP 2017 · Additional VEP course citations (not independently linked here): Harding et al. 1990; Goto et al. 2007; Chung et al. 2012; Kodama et al. 2010; Neuloh 2010; Masui 2006;55:692-8; Watson & Shah 2000. Additional MEP course citations (not independently linked here): Jahangiri FR, TCeMEP course lecture; Jahangiri et al. 2012, 2014, 2016, 2017, 2018, 2019, 2023; Nadeem et al. 2023; Shils & Deletis 2014. Additional EEG course citations (not independently linked here): Mora M, IONM EEG course lecture; Hirsch et al. 2021 (ACNS Standardized Critical Care EEG Terminology); Sinha et al. 2016; ASET 1998; Klem GH et al. 2019; Date A et al. 2020; Mora et al. 2022. Additional SSEP course citations (not independently linked here): Gale C, SSEP IONM course lecture; Nash C 1977 (origin of the 50% rule); Nuwer & Dawson 1984; Acharya et al. 2016 (ACNS Guideline 2, electrode nomenclature); Blum & Rutkove, The Clinical Neurophysiology Primer; Erwin & Erwin 1993. Additional EMG course citations (not independently linked here): Gale C, IO EMG course lecture; Calancie et al 1994; Maguire et al 1995; Glassman et al 1995; Lenke et al 1995; Clements et al 1996; Toleikis 2002; Djurasovic et al 2005; Raynor et al 2001; Kuklo et al 2002; Samdani et al 2011; Szkiladz et al 1995; Wierzbowski et al 2003 & 2008; Skinner et al 2008; Minahan et al; Gundanna et al 2003. Additional BAEP / VEP citations: ACNS 11C (intraoperative BAEP); ASNM AEP position statement; Kodama / Sasaki 2017 (flash VEP under GA); Clinical utility & limitations of intraoperative VEP (PLOS One 2015).