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; 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)
🚩 Don’t Miss — Test-Day Priorities
- 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.
🔍 Buzzwords & Pathognomonic FindingsNCS / 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.
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 H-reflex via median nerve stimulation (tests C6–C7, primarily 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) |
Board Pearl
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 → >10% decrement between 1st and 4th (or 5th) response (typically maximal at 4th — U-shaped envelope)
- 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, painful) or post-exercise → massive Ca2+ influx at presynaptic terminal → increment in presynaptic disorders; brief 10-sec maximal voluntary contraction is the practical equivalent
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 ≥60% (classic threshold >100%; modern AANEM threshold ≥60%) on high-frequency RNS or 10-sec brief exercise. | Increment 20–40% (small) |
| SFEMG jitter | Increased (most sensitive test) | Increased | Increased |
| Most sensitive test | SFEMG (~95–99%) | Post-exercise CMAP increment | EMG + RNS |
Board Pearl
LEMS = low baseline CMAP + ≥60% increment post-exercise (classic threshold >100%; modern AANEM threshold ≥60%) on high-frequency RNS or 10-sec brief 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.
Clinical Pearl
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; initial positive deflection (distinguishes from end-plate spikes which have initial negative deflection); 1–5 ms duration, regular firing 1–50 Hz. | "Rain on a tin roof" | Denervation (lower motor neuron, radiculopathy, peripheral nerve injury, plexopathy), inflammatory myopathy, severe myopathies, channelopathies. Note: severe botulism may rarely cause functional denervation. |
| 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" | Myotonic dystrophy (DM1/DM2), myotonia congenita (CLCN1), paramyotonia (SCN4A), hyperKPP, acid maltase deficiency (Pompe — myotonic discharges WITHOUT clinical myotonia, paraspinal-predominant), statin/colchicine myopathy, acid maltase |
| 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 — VGKC-complex antibodies (CASPR2 most common); Caspr2 also seen in Morvan syndrome / limbic encephalitis; LGI1 more limbic encephalitis. Thymoma, post-radiation. |
Board Pearl — EMG Sound Mnemonics
- Myotonic discharge — "dive bomber" (waxing/waning frequency and amplitude); triggered by needle movement; seen in DM1/DM2, myotonia congenita, paramyotonia, Pompe (paraspinal).
- Complex repetitive discharges (CRDs) — "jackhammer / motor" (uniform, abrupt onset/offset, NO waxing/waning); chronic neurogenic processes and chronic myopathies.
- Myokymia — "marching soldiers" (rhythmic bursts of grouped MUAPs); think radiation plexopathy, GBS facial myokymia, MS, episodic ataxia 1 (KCNA1).
- Fasciculations — "popcorn" (random, infrequent, larger amplitude than fibs); benign fasciculations, ALS, radiculopathy.
- Fibrillations / positive sharp waves — like rain on a tin roof; ongoing denervation.
💎 Board Pearl — Standard NCS Misses
- Routine NCS evaluates only large myelinated fibers (Aα and Aβ). Small-fiber neuropathies (autonomic dysfunction, burning pain, normal NCS) require QSART (quantitative sudomotor axon reflex test) or skin biopsy (PGP9.5 intraepidermal nerve fiber density) for diagnosis. Causes: diabetes/IGT, amyloid (TTR), Sjögren, Fabry, idiopathic, HIV, vasculitis.
- Steroid myopathy is type-II-predominant atrophy and may have normal CK and normal or nonspecific EMG despite proximal weakness; muscle biopsy or clinical context may be more revealing than routine EMG. (Note: do NOT claim "EMG predominantly evaluates type 1 fibers" as a physiologic rule — needle EMG samples motor-unit electrical behavior, and recruitment depends on effort, muscle, and motor-unit activation, not a direct fiber-type assay.) Proximal weakness with normal EMG and normal CK in a patient on chronic steroids = steroid myopathy until proven otherwise.
💎 Board Pearl — Acute Denervation Timeline
After acute nerve injury, EMG findings evolve in a predictable sequence:
- Immediately: reduced recruitment on voluntary effort (only finding for the first ~10 days — high-yield board point).
- Day 7–10 (paraspinals) / 2–3 weeks (proximal limb) / 3–6 weeks (distal limb): fibrillations and positive sharp waves appear (spontaneous activity of denervated fibers).
- 3–6 months: nascent (reinnervation) MUAPs — unstable, polyphasic, low amplitude, short duration.
- Years (chronic): giant polyphasic MUAPs (chronic reinnervation); fibs may persist if reinnervation incomplete.
An "EMG too early" (within first 10 days) will look falsely normal except for reduced recruitment — tell the referring clinician to wait at least 2–3 weeks for the full picture in acute injury.
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"
Clinical Pearl
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) | First MUP firing >15–20 Hz before second is recruited (recruitment ratio >10; normal ~5); 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 |
Board Pearl
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 | Sensory NCS usually normal; CMAP may be low (abnormal SNAPs → search for mimics/coexisting neuropathy, not automatic exclusion) | Widespread fibs + fascs; large MUPs; reduced recruitment in ≥3 regions | Widespread denervation with sensory usually normal = motor neuron disease pattern; abnormal SNAPs do NOT automatically exclude ALS |
| 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. Median motor DML >4.4 ms; median sensory peak latency >3.5 ms at 14 cm; median-ulnar palmar sensory difference >0.5 ms (most sensitive) | 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 | >10% decrement between 1st and 4th (or 5th) response on RNS (typically maximal at 4th — U-shaped envelope) |
| NMJ disorder (LEMS) | Low baseline CMAP; ≥60% increment post-exercise (classic >100%; modern AANEM ≥60%) | Normal or mildly abnormal routine EMG | Low CMAP + dramatic facilitation = presynaptic defect |
Board Pearl
ALS pattern: widespread active/chronic denervation with no conduction block, and sensory NCS usually normal — but abnormal SNAPs should trigger a search for ALS mimics or coexisting neuropathy (entrapment, diabetic/age-related, vasculitic), not automatic exclusion. 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; paraspinal fibrillations appear |
| 2–3 weeks | Low or absent distal responses | Proximal limb fibs prominent |
| 3–6 weeks | Low or absent distal responses | Distal limb fibs; maximal denervation findings |
| 3–6 months | May see nascent CMAPs returning | Nascent (reinnervation) MUPs: unstable (varying morphology shot-to-shot), low amplitude, short duration, highly polyphasic; 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 (7–10 days), proximal limb (2–3 weeks), distal limb (3–6 weeks)
Board Pearl
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 + ≥10% decrement at low-rate RNS. LEMS: low CMAP + ≥60% increment on high-rate RNS or post-exercise (classic threshold >100%; modern AANEM cutoff ≥60%). |
| 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 |
Board Pearl
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.
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