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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; 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) |
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.
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.
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).