CNIM cheat sheet

Upper-limb SSEP pathway: median nerve → brachial plexus → C6-C8 dorsal roots → dorsal columns → nucleus cuneatus → medial lemniscus → VPL thalamus → primary somatosensory cortex.

Corticospinal tract: motor cortex → corona radiata → posterior limb of internal capsule → cerebral peduncle → basis pontis → medullary pyramid → decussation → lateral corticospinal tract.

BAEP generators: wave I distal eighth nerve; wave II proximal eighth nerve; wave III cochlear nucleus; wave IV superior olivary complex; wave V inferior colliculus/lateral lemniscus.

EEG frequency bands: delta <4 Hz; theta 4-7.9 Hz; alpha 8-13 Hz; beta >13 Hz.

Ohm's law: V = I × R; power: P = I²R. Low electrode impedance reduces thermal noise and improves signal-to-noise ratio.

Differential amplifiers reject common-mode signals; higher common-mode rejection ratio (CMRR) improves rejection of 60 Hz and other shared interference.

Typical sweep windows: BAEP 10 ms; upper-limb SSEP 50 ms; lower-limb SSEP 100 ms; MEP 100 ms.

Fasciculus gracilis carries lower-limb proprioception and vibration medially; fasciculus cuneatus carries upper-limb fibers laterally in the dorsal columns.

Volatile anesthetics cause dose-dependent cortical SSEP amplitude reduction and latency prolongation; BAEPs are relatively resistant.

MEPs are more sensitive to anesthetics than SSEPs; volatile agents, propofol, and nitrous oxide can suppress or abolish MEPs.

Propofol produces dose-dependent EEG slowing and burst suppression and suppresses MEPs and cortical SSEPs.

Nitrous oxide above 50% can depress MEP and cortical SSEP amplitude; reduce or discontinue when MEPs are critical.

Neuromuscular blockade abolishes MEP and EMG but does not directly block SSEP or BAEP; monitor TOF when blockade is used.

Ketamine can increase fast EEG activity and may preserve or enhance MEP amplitude; it is used as an adjunct in some MEP cases.

Hypothermia prolongs evoked potential latencies and reduces amplitudes; document core temperature with every significant change.

Opioids at usual doses have minimal effect on SSEP and BAEP; high doses can produce EEG slowing.

Median nerve SSEP: wrist stimulation, 0.2 ms pulse, 3-5 Hz, supramaximal intensity; record Erb's point, C7, and contralateral scalp.

Transcranial MEP: train of 5-7 pulses, 50-500 µs duration, 1-4 ms interpulse interval; record CMAP from target muscles.

BAEP: 80-100 dB nHL clicks, 10-20 Hz rate, 10 ms window, 1000-2000 averages; monitor waves I, III, V and I-V interpeak latency.

Triggered EMG pedicle screw thresholds: below about 6 mA is concerning for breach; above 10-12 mA is generally reassuring; impedance and relaxant affect values.

Spontaneous EMG: brief neurotonic bursts suggest nerve irritation; sustained high-frequency trains are more concerning for nerve injury.

Median nerve SSEP phase reversal across the central sulcus identifies the sensorimotor boundary during cortical mapping.

EEG ischemia signs: loss of fast activity, increased slowing, and amplitude reduction; compare with baseline and systemic factors.

Burst suppression: isoelectric periods with intermittent bursts; cortical SSEP and MEP may be absent, so interpret with anesthetic depth.

Check all electrode impedances before incision; target <5 kΩ and recheck after positioning and draping.

Use a 60 Hz notch filter only when necessary; it can mask real signal and should not replace fixing ground, reference, or electrode contact.

Sudden signal loss: verify stimulator output, electrode connections, impedance, anesthesia, blood pressure, temperature, and surgical activity before assuming injury.

Cephalic or ear references are common for SSEP and BAEP referential montages; keep reference choice and montage constant across the case.

Electrocautery creates broadband artifact; pause acquisition and do not interpret evoked potentials during cautery.

Hypotension can reduce cortical SSEP amplitude; record mean arterial pressure at the time of change and communicate with anesthesia.

For MEP, confirm stable anesthetic and neuromuscular blockade status; changes in TOF or anesthetic depth can mimic MEP loss.

Positioning can compress peripheral nerves and the brachial plexus; pad pressure points and reassess signals after final positioning.

Document baseline parameters: modality, montage, stimulation settings, limb side, anesthetic regimen, temperature, blood pressure, and signal reproducibility.

For any critical change, record time, modality, change, suspected cause, intervention, and who was notified with response.

Use closed-loop communication: state the message, have the receiver repeat it back, and confirm before action.

Share only minimum necessary protected health information and follow institutional privacy policy.

Verify patient identity, procedure, and laterality before stimulation; compare left versus right and document side.

If a concern is unresolved, escalate through the chain of command and document each step.

Record artifacts and technical problems that affect interpretation, including cautery, movement, and poor impedance.

Avoid unapproved abbreviations and ambiguous terms; use standardized modality names and units.