NCS/EMG Basics
NCS/EMG Basics
What Do You Need to Know?
- 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 + normal sensory), GBS (demyelinating + absent F-waves), carpal tunnel (prolonged median DL)
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
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 (<70% lower limit of normal) |
| Distal latency (DL) | Conduction time across distal nerve segment | Distal demyelination (>130% upper limit of normal) |
| 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) |
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 | <70% LLN (markedly slow) | Normal or mildly slow (>70% LLN) |
| Distal latency | >130% ULN (prolonged) | 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 |
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.
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.
Late Responses
F-Wave vs H-Reflex
| Feature | F-Wave | H-Reflex |
|---|---|---|
| Pathway | Antidromic motor → anterior horn cell → orthodromic return | Ia afferent → spinal cord → motor neuron (monosynaptic reflex arc) |
| Equivalent to | No clinical reflex equivalent | Electrical equivalent of the ankle jerk (S1) |
| Latency | Variable (different anterior horn cells each time) | Consistent (same reflex arc) |
| Morphology | Variable shape and amplitude | Consistent shape |
| Stimulus intensity | Supramaximal | Submaximal (disappears with supramaximal stim) |
| Nerve tested | Any motor nerve (median, ulnar, peroneal, tibial) | Tibial nerve (S1 arc); less commonly FCR (C6–C7) |
| Tests | Proximal nerve segments, roots, anterior horn cells | S1 root, Ia afferent, motor neuron |
| Abnormal in | GBS (early finding), radiculopathy, proximal neuropathy | S1 radiculopathy, polyneuropathy, elderly (absent bilaterally) |
F-waves are often the earliest abnormality in GBS — prolonged or absent when distal NCS are still normal (because demyelination begins at roots/proximal nerve). H-reflex = S1; absent unilateral H-reflex with a normal ankle jerk suggests early or mild S1 radiculopathy.
Repetitive Nerve Stimulation (RNS)
Physiology
- Low-rate RNS (2–3 Hz) — depletes readily releasable ACh vesicles at NMJ
- Normal NMJ has a large safety factor → no decrement
- In MG (postsynaptic defect) → reduced safety factor → decrement >10% at 4th–5th response
- Post-exercise facilitation — brief exercise increases ACh release → temporary repair of decrement (in MG) or marked increment (in LEMS)
- High-rate RNS (20–50 Hz) or post-exercise → massive Ca2+ influx at presynaptic terminal → increment in presynaptic disorders
Lambert-Eaton vs MG vs Botulism
| Feature | Myasthenia Gravis | Lambert-Eaton (LEMS) | Botulism |
|---|---|---|---|
| Defect | Postsynaptic (AChR antibodies) | Presynaptic (VGCC antibodies) | Presynaptic (toxin blocks ACh release) |
| Baseline CMAP | Normal | Low | Low |
| Low-rate RNS (2–3 Hz) | Decrement >10% | May show decrement | May show decrement |
| Post-exercise / high-rate | Repair of decrement | Increment >100% | Increment 20–40% (small) |
| SFEMG jitter | Increased (most sensitive test) | Increased | Increased |
| Most sensitive test | SFEMG (~95–99%) | Post-exercise CMAP increment | EMG + RNS |
LEMS = low baseline CMAP + >100% increment post-exercise. MG = normal baseline CMAP + >10% decrement at low-rate RNS. Botulism shows a low baseline CMAP with only a small increment (20–40%). The magnitude of the increment separates LEMS from botulism.
Always stop acetylcholinesterase inhibitors (e.g., pyridostigmine) at least 12 hours before RNS testing in suspected MG — the drug can mask the decrement and produce a false-negative result.
Needle EMG — Spontaneous Activity
| Finding | Description | Sound | Associated Conditions |
|---|---|---|---|
| Insertional activity (increased) | Prolonged bursts with needle movement | Brief runs of spikes | Denervation, inflammatory myopathy (decreased in fibrosis/fatty replacement) |
| Fibrillation potentials | Spontaneous single-fiber discharge; biphasic/triphasic; regular firing | "Rain on a tin roof" | Denervation (onset 2–3 weeks), inflammatory myopathy, muscular dystrophy, NMJ disorders |
| Positive sharp waves (PSWs) | Initial positive deflection then slow negative; regular | Dull "thud" | Same significance as fibrillations |
| Fasciculation potentials | Spontaneous motor unit discharge; irregular firing rate | "Popcorn" | ALS, radiculopathy, benign fasciculations, cramp-fasciculation syndrome |
| Myotonic discharges | Waxing AND waning frequency and amplitude; triggered by needle movement | "Dive bomber" | DM1/DM2, myotonia congenita, paramyotonia congenita, hyperkalemic periodic paralysis |
| Complex repetitive discharges (CRDs) | Polyphasic; regular; abrupt start/stop; NO waxing/waning | "Jackhammer" / "motorcycle" | Chronic denervation, chronic myopathy, radiculopathy |
| Myokymic discharges | Grouped, repetitive bursts of the same MUP; semi-rhythmic | "Marching soldiers" | Radiation plexopathy, GBS, MS, facial myokymia (brainstem glioma) |
| Neuromyotonic discharges | Very high frequency (150–300 Hz); decrementing | "Ping" / musical | Isaacs syndrome (anti-CASPR2), thymoma, post-radiation |
Myotonic discharge = waxing/waning (dive bomber). CRD = NO waxing/waning (jackhammer). Both are triggered by needle movement, but only myotonic discharges change in frequency and amplitude. Myokymia on EMG → think radiation injury or GBS. Neuromyotonia → Isaacs syndrome.
Motor Unit Potentials (MUPs)
Normal MUP Parameters
- Amplitude — 200 µV to 5 mV (muscle-dependent)
- Duration — 5–15 ms (increases with age)
- Phases — 2–4 phases (>4 = polyphasic; up to 10–15% polyphasic MUPs is normal)
Neuropathic vs Myopathic MUPs
| Feature | Neuropathic (Chronic Reinnervation) | Myopathic |
|---|---|---|
| Amplitude | Large / giant | Small / low |
| Duration | Long | Short |
| Phases | Polyphasic (due to collateral sprouting) | Polyphasic (due to fiber dropout/desynchrony) |
| Recruitment | Reduced (fewer MUPs firing fast) | Early / rapid (many small MUPs at low force) |
| Mechanism | Collateral sprouting → more fibers per motor unit | Loss of muscle fibers → fewer fibers per motor unit |
| Stability | May be unstable early (nascent), stable late | May be unstable (if active disease) |
Memory Aid
- Neuropathic = "LARP" — Large Amplitude, Reduced Recruitment, Polyphasic
- Myopathic = "SERF" — Small, Early recruitment, Rapid firing, Fractionated (polyphasic)
- "Sick nerve = big units; sick muscle = small units"
Inclusion body myositis (IBM) is the classic exception — it shows mixed myopathic AND neurogenic MUPs (long-duration polyphasic units in a myopathy). This mixed pattern on EMG is highly characteristic and should prompt consideration of IBM in the right clinical context.
Recruitment
Recruitment Patterns
| Pattern | Description | Seen In |
|---|---|---|
| Normal | Recruitment ratio ~5:1 (firing rate of first MUP when second is recruited) | Normal muscle |
| Reduced (neurogenic) | Fewer MUPs firing at high rates (>15–20 Hz before next MUP recruited); incomplete interference pattern | Neuropathy, radiculopathy, ALS, motor neuron disease |
| Early / rapid (myopathic) | Many small MUPs recruited at low force levels; full interference pattern with minimal effort | Myopathy (any cause) |
| Poor activation (central) | Few MUPs firing at low rates; normal MUP morphology; patient cannot increase firing rate | UMN lesion, pain, poor effort |
Poor activation (UMN or effort-related) can mimic neurogenic recruitment. The key distinction: in neurogenic reduced recruitment, MUPs fire fast (>15–20 Hz) before the next is recruited. In poor activation, MUPs fire slowly and the patient cannot drive them faster.
Disease Pattern Recognition
Master Table
| Disease | NCS Findings | EMG Findings | Key Distinguishing Feature |
|---|---|---|---|
| ALS | Normal sensory NCS; CMAP may be low | Widespread fibs + fascs; large MUPs; reduced recruitment in ≥3 regions | Widespread denervation + normal sensory = motor neuron disease |
| GBS (AIDP) | Demyelinating: slow CV, prolonged DL, conduction block, temporal dispersion | Fibs if secondary axonal loss; reduced recruitment | Absent/prolonged F-waves early (often first abnormality) |
| CIDP | Demyelinating (symmetric): prolonged DL >130% ULN, slow CV, conduction block | Chronic neurogenic changes if axonal loss | Symmetric, chronic, uniform demyelination; responds to treatment |
| Carpal tunnel syndrome | Prolonged median DL; low median SNAP; slow median sensory CV across wrist; normal ulnar | Fibs in APB (severe); neurogenic MUPs in APB | Median vs ulnar comparison studies (most sensitive) |
| Radiculopathy | Normal NCS (including normal SNAP) | Fibs in myotomal distribution; paraspinal fibs; neurogenic MUPs | Normal SNAP + abnormal paraspinals = preganglionic lesion |
| Myopathy (non-inflammatory) | Normal NCS (CMAP may be low if severe) | Small, short, polyphasic MUPs; early recruitment; no fibs | No spontaneous activity (vs inflammatory which has fibs) |
| Inflammatory / necrotizing myopathy | Normal NCS | Myopathic MUPs + fibs/PSWs ("irritable myopathy"); CRDs | Fibrillations in a myopathic pattern = active muscle fiber necrosis |
| NMJ disorder (MG) | Normal routine NCS; decrement on low-rate RNS | Normal routine EMG; increased jitter on SFEMG | Decrement >10% at 4th–5th response on RNS |
| NMJ disorder (LEMS) | Low baseline CMAP; >100% increment post-exercise | Normal or mildly abnormal routine EMG | Low CMAP + dramatic facilitation = presynaptic defect |
ALS requires normal sensory NCS. If sensory studies are abnormal, reconsider the diagnosis. MMN mimics ALS but shows motor conduction block with normal sensory — and is treatable with IVIG. Radiation plexopathy is distinguished from neoplastic plexopathy by the presence of myokymic discharges.
Denervation Timeline
EMG Changes After Nerve Injury
| Time After Injury | NCS Findings | EMG Findings |
|---|---|---|
| 0–7 days | Conduction block at lesion; distal responses still normal | Reduced recruitment only; NO fibrillations |
| 7–10 days | Distal CMAP/SNAP begin to drop (Wallerian degeneration) | Reduced recruitment; fibs starting in proximal muscles |
| 2–3 weeks | Low or absent distal responses | Fibs/PSWs prominent in proximal muscles; paraspinals ~10 days |
| 4–6 weeks | Low or absent distal responses | Fibs/PSWs reach distal muscles; maximal denervation findings |
| 3–6 months | May see nascent CMAPs returning | Nascent (reinnervation) MUPs: small, polyphasic, unstable; fibs persist |
| 6–12 months | CMAP improving | Large polyphasic MUPs (collateral sprouting); reduced recruitment; fibs decreasing |
| Years (chronic stable) | May normalize or remain low | Giant MUPs; reduced recruitment; NO fibs (stable reinnervation) |
Interpreting the Timeline
- Fibs WITHOUT large MUPs → acute/ongoing denervation
- Fibs WITH large MUPs → chronic process with ongoing denervation
- Large MUPs WITHOUT fibs → chronic, stable (old injury, fully reinnervated)
- Fibs appear proximal to distal — paraspinals first (~10 days), proximal limb (2–3 weeks), distal limb (4–6 weeks)
EMG performed too early (<2–3 weeks) after nerve injury will miss fibrillations. The optimal timing for initial EMG is 3–4 weeks after injury. If fibrillations are present in the first week, suspect a pre-existing or chronic process rather than the acute injury.
Quick Reference
Summary — NCS/EMG at a Glance
| Question | Answer |
|---|---|
| Axonal vs demyelinating? | Axonal = low amplitude. Demyelinating = slow CV, prolonged DL, conduction block. |
| Preganglionic vs postganglionic? | Normal SNAP = preganglionic (radiculopathy). Abnormal SNAP = postganglionic. |
| Radiculopathy vs plexopathy? | Radiculopathy: normal SNAP + abnormal paraspinals. Plexopathy: abnormal SNAP + normal paraspinals. |
| Neuropathic vs myopathic MUPs? | Neuropathic: large, long, reduced recruitment. Myopathic: small, short, early recruitment. |
| MG vs LEMS on RNS? | MG: normal CMAP + decrement. LEMS: low CMAP + >100% increment. |
| When do fibs appear? | 2–3 weeks after injury (proximal muscles first). |
| Dive bomber sound? | Myotonic discharge (waxing/waning). |
| Myokymia on EMG? | Radiation plexopathy, GBS, MS. |
| Most sensitive test for MG? | Single-fiber EMG (SFEMG) — ~95–99% sensitivity. |
| Earliest finding in GBS? | Absent or prolonged F-waves. |
Spontaneous Activity Sound Guide
| Sound | Finding | Think Of |
|---|---|---|
| "Dive bomber" (waxing/waning) | Myotonic discharge | DM1/DM2, myotonia congenita |
| "Marching soldiers" (grouped bursts) | Myokymia | Radiation injury, GBS |
| "Ping" (high-frequency, decrementing) | Neuromyotonia | Isaacs syndrome |
| "Jackhammer" (abrupt start/stop, no wax/wane) | CRD | Chronic denervation/myopathy |
| "Rain on tin roof" | Fibrillations | Denervation, inflammatory myopathy |
| "Popcorn" (irregular) | Fasciculations | ALS, benign fasciculations |
IBM shows mixed myopathic AND neurogenic MUP features — this is unique among myopathies and a favorite board question. Long-duration polyphasic MUPs in a patient with finger flexor and quadriceps weakness should raise suspicion for IBM.
References
- Preston DC, Shapiro BE. Electromyography and Neuromuscular Disorders: Clinical-Electrophysiologic-Ultrasound Correlations. 4th ed. Elsevier; 2021.
- Dumitru D, Amato AA, Zwarts MJ. Electrodiagnostic Medicine. 2nd ed. Hanley & Belfus; 2002.
- American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM). Practice guidelines for electrodiagnostic medicine.
- Katirji B. Electromyography in Clinical Practice. 3rd ed. Oxford University Press; 2018.
- Continuum (AAN). Neuromuscular and Electrodiagnostic Medicine review articles.