NCS/EMG Basics
NCS/EMG Basics
What You'll Learn
- Motor NCS (CMAP) — stimulate nerve, record muscle; amplitude reflects motor axon number
- Sensory NCS (SNAP) — stimulate nerve, record nerve; normal SNAP in radiculopathy (preganglionic)
- Demyelinating vs axonal — slow CV/conduction block vs low amplitude/fibrillations
- Late responses — F-wave (proximal motor nerve) vs H-reflex (S1 reflex arc)
- RNS — decrement in MG, increment in LEMS; know the comparison table
- Spontaneous activity — fibrillations (denervation, 2–3 weeks), myotonic discharges (dive bomber), myokymia (radiation)
- MUP analysis — neuropathic = large, long, reduced recruitment; myopathic = small, short, early recruitment
- Disease patterns — ALS (widespread denervation; sensory NCS usually normal — abnormal SNAPs should trigger a search for mimics/coexisting neuropathy, not automatic exclusion), GBS (demyelinating + absent F-waves), carpal tunnel (prolonged median DL)
HighYield Pearls
- SNAP preserved in radiculopathy: lesion is preganglionic (DRG intact) → normal SNAP with denervation on needle EMG localizes to root; reduced SNAP shifts localization to plexus or peripheral nerve.
- Demyelinating signature: prolonged distal latency (>125% ULN), slowed CV (<75% LLN), temporal dispersion, conduction block, prolonged/absent F-waves — think GBS, CIDP, CMT1, MMN.
- Axonal signature: reduced CMAP/SNAP amplitudes with relatively preserved CV and DL; fibs/PSWs on needle EMG — think diabetic, toxic, ALS, vasculitic neuropathy.
- Cold limb pitfall: cool limb falsely prolongs distal latency, slows CV, and increases amplitude/duration — warm limb to ≥32°C before declaring demyelination.
- RNS — MG vs LEMS: 3 Hz slow RNS decrement >10% = postsynaptic (MG); >60–100% increment after 10 s exercise or 20–50 Hz tetanic = presynaptic (LEMS, botulism).
- Single-fiber EMG is most sensitive NMJ test: increased jitter ± blocking — positive when RNS is normal in ocular/mild MG; not specific (also abnormal in ALS, myopathy).
- Fibs + PSWs = active denervation: appear 2–3 weeks after axon loss; absent acutely (don’t exclude radiculopathy in week 1) and absent in pure demyelination/conduction block.
- Myotonic discharges (“dive bomber”): waxing/waning amplitude + frequency — DM1/DM2, myotonia congenita, paramyotonia, hyperkalemic periodic paralysis, Pompe, acid maltase deficiency, IBM (rare).
- Neurogenic MUAP: large-amplitude, long-duration, polyphasic, reduced recruitment (fast firing of few units) — reinnervation pattern; myopathic MUAP: small, short, polyphasic, early recruitment with full effort.
- F-wave vs H-reflex: F-wave = antidromic motor backfire, any motor nerve, tests proximal motor conduction (GBS earliest finding); H-reflex = monosynaptic Ia→α-motor reflex, tibial→soleus, tests S1 root.
🔍 Quick ReferenceNCS / late responses · EMG signals · Disease signatures
NCS / late responses
- Prolonged distal latency + slowed CV + temporal dispersion + conduction block → acquired demyelinating neuropathy (GBS, CIDP, MMN)
- Uniformly slowed CV without temporal dispersion or block → hereditary demyelination (CMT1)
- Low CMAP/SNAP amplitude with preserved CV → axonal neuropathy
- Absent or prolonged F-waves with otherwise normal NCS → early GBS (proximal demyelination)
- Absent H-reflex with Achilles areflexia → S1 radiculopathy or length-dependent peripheral neuropathy
- Blink reflex R1 delayed → pontine/trigeminal lesion; R2 delayed → lateral medullary or afferent V lesion
EMG signal patterns
- Fibrillation potentials + positive sharp waves at rest → active denervation (≥2–3 weeks post-axonal injury)
- Complex repetitive discharges (CRDs) → chronic denervation/reinnervation (chronic radiculopathy, IBM, chronic myopathy)
- Myotonic discharges — “dive bomber” waxing/waning → myotonic dystrophy, myotonia congenita, paramyotonia, hyperkalemic PP, Pompe
- Myokymic discharges — “marching soldiers” grouped bursts → radiation plexopathy, Isaacs syndrome, CASPR2 antibodies, MS (facial myokymia)
- Neuromyotonia — continuous high-frequency (150–300 Hz) motor unit firing → Isaacs syndrome (acquired neuromyotonia)
- Fasciculation potentials, widespread + chronic neurogenic MUAPs in ≥3 regions → ALS (benign fasciculations have normal MUAPs and no denervation)
- Reduced recruitment with full central drive → neurogenic process (axon loss or conduction block); poor recruitment with submaximal firing rates → central/UMN process or pain/effort
- Early (full) recruitment of small, short, polyphasic MUAPs → myopathy
Disease signatures
- 3 Hz RNS decrement >10% with post-exercise facilitation then exhaustion → myasthenia gravis (postsynaptic NMJ)
- Low baseline CMAP with >60–100% increment after brief exercise or 50 Hz stim → Lambert-Eaton (LEMS) or botulism (presynaptic NMJ)
- Increased jitter ± blocking on single-fiber EMG → NMJ disorder (most sensitive test for MG)
- Widespread fibs/PSWs + chronic neurogenic MUAPs + sensory NCS usually normal → motor neuron disease (ALS) — abnormal SNAPs should trigger a search for ALS mimics or coexisting neuropathy, not automatic exclusion
- Demyelinating NCS + absent/prolonged F-waves + albuminocytologic dissociation (typical but may be absent early — CSF protein normal in ~50% during week 1, more often elevated by week 2; normal early CSF does NOT rule out GBS) → Guillain-Barré syndrome
- Prolonged median distal motor + sensory latencies across the wrist with normal ulnar → carpal tunnel syndrome
- Normal SNAP with denervation in a myotomal distribution → radiculopathy (preganglionic)
NCS Basics
Motor vs Sensory NCS
| Feature | Motor NCS (CMAP) | Sensory NCS (SNAP) |
|---|---|---|
| Stimulate | Nerve | Nerve |
| Record | Muscle (surface electrode) | Nerve (ring or bar electrode) |
| Waveform | CMAP (compound muscle action potential) | SNAP (sensory nerve action potential) |
| Amplitude reflects | Number of motor axons + muscle fibers | Number of sensory axons |
| Normal amplitude | >4–5 mV (nerve-dependent) | >10–20 µV (nerve-dependent) |
| Parameters measured | Distal latency, amplitude, CV, F-wave | Latency, amplitude, CV |
| Key clinical use | Motor axon loss, NMJ disorders, myopathy | Pre- vs postganglionic localization |
Orthodromic vs Antidromic Recording
- Orthodromic — stimulate distally, record proximally (direction of physiologic conduction)
- Antidromic — stimulate proximally, record distally (against physiologic direction)
- Antidromic SNAPs are larger (easier to obtain) but may have volume-conducted CMAP contamination
- Both yield equivalent latency and conduction velocity values
Board Pearl
SNAP is preserved in radiculopathy because the lesion is preganglionic (dorsal root ganglion is intact). SNAP is reduced in plexopathy and peripheral neuropathy (postganglionic lesions). This is the single most important NCS localization principle.
Key NCS Parameters
| Parameter | What It Measures | Abnormal In |
|---|---|---|
| Amplitude | Number of functioning axons (axon count/integrity) | Axonal loss, conduction block (distal to block) |
| Conduction velocity (CV) | Speed of fastest fibers (myelin integrity) | Demyelination (<75% LLN (or <70% if CMAP amplitude >80% LLN; <80% LLN if amplitude reduced per EFNS/PNS criteria).) |
| Distal latency (DL) | Conduction time across distal nerve segment | Distal demyelination (>125% ULN (>150% ULN if distal CMAP <80% LLN).) |
| Temporal dispersion | Synchrony of conduction across fibers (differential slowing) | Acquired demyelination (>30% duration increase proximal vs distal) |
| Conduction block | Focal inability to conduct across a segment | Focal demyelination (>50% amplitude drop proximal vs distal) |
Clinical Pearl
Conduction block produces weakness without atrophy because the axons remain intact — they simply cannot conduct past the demyelinated segment. This explains why patients with GBS or MMN can have severe weakness but preserved muscle bulk early on.
Demyelinating vs Axonal Patterns
| Feature | Demyelinating | Axonal |
|---|---|---|
| Conduction velocity | <75% LLN (or <70% if CMAP amplitude >80% LLN; <80% LLN if amplitude reduced per EFNS/PNS criteria). | Normal or mildly slow (>75% LLN) |
| Distal latency | >125% ULN (>150% ULN if distal CMAP <80% LLN). | Normal or mildly prolonged |
| Amplitude | Preserved early; low late (secondary axonal loss) | Low (proportional to axon loss) |
| Temporal dispersion | Present | Absent |
| Conduction block | Present (>50% amp drop) | Absent |
| F-wave latency | Prolonged or absent | Normal or mildly prolonged |
| Fibrillations on EMG | Less prominent (unless secondary axonal loss) | Prominent |
Clinical Examples
| Demyelinating | Axonal |
|---|---|
| GBS (AIDP) | GBS (AMAN, AMSAN) |
| CIDP | Diabetic polyneuropathy |
| CMT1 (hereditary) | CMT2 (hereditary) |
| MMN (multifocal motor neuropathy) | Toxic/metabolic neuropathies |
| Anti-MAG neuropathy | Vasculitic neuropathy |
Board Pearl
Temporal dispersion and conduction block indicate acquired (non-uniform) demyelination. Hereditary demyelinating neuropathies (e.g., CMT1) show uniformly slow CV without conduction block or temporal dispersion. This distinction separates acquired from inherited causes.
Board Pearl
Severe axonal loss can mimic demyelination — if very few axons remain, the fastest fibers are lost and CV appears slow. Always check whether low amplitude accounts for the slow velocity before diagnosing demyelination.
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