EMG/NCS Patterns
EMG/NCS Patterns in Neuromuscular Disease
What Do You Need to Know?
- Axonal vs demyelinating NCS: axonal → reduced amplitudes with preserved velocities; demyelinating → slowed velocities (<70% LLN), prolonged distal latencies, conduction block, temporal dispersion
- Conduction block = acquired demyelination: >50% CMAP amplitude/area drop = definite conduction block (EFNS/PNS 2021); >30% drop = possible conduction block when combined with other demyelinating features; seen in CIDP, MMN, GBS — NOT in hereditary (CMT1)
- Neurogenic vs myopathic MUAPs: neurogenic = large, long, polyphasic, reduced recruitment; myopathic = small, short, polyphasic, early recruitment
- RNS patterns: MG = ≥10% decrement at 2–3 Hz (postsynaptic); LEMS = ≥60% increment at 20–50 Hz (AANEM current standard; historical threshold was 100%) (presynaptic); botulism = increment (less dramatic than LEMS)
- SFEMG: most sensitive test for NMJ disorders (~95% for generalized MG; ~90% for ocular MG when clinically weak muscle tested); measures jitter and blocking — but NOT specific (abnormal in reinnervation too)
- Fibrillations ≠ denervation exclusively: also seen in inflammatory myopathies, necrotizing myopathies, muscular dystrophies, acid maltase deficiency
- Localization keys: paraspinal fibrillations → root; reduced SNAP → distal to DRG (plexus/nerve); normal SNAP + abnormal CMAP → motor neuron/root/NMJ/myopathy
- Temperature trap: cold limb → artificially slowed velocities, prolonged latencies, and increased CMAP amplitude — always warm to ≥32°C before testing
🚩 Don’t Miss — Test-Day Priorities
- Demyelinating NCS quartet: prolonged distal motor latencies + slowed CV (<70% LLN) + temporal dispersion + conduction block ± abnormal/absent F-waves — defines acquired demyelination (CIDP, GBS, MMN)
- Axonal NCS: reduced CMAP/SNAP amplitudes with preserved (or only mildly slowed) CV; F-waves normal or absent if severe loss
- Conduction block at non-entrapment sites: hallmark of MMN (pure motor, asymmetric) and CIDP/AIDP — NEVER seen in hereditary demyelinating neuropathies (CMT1A)
- Uniform vs multifocal slowing: uniform/symmetric slowing → hereditary demyelinating (CMT1A); multifocal slowing with conduction block/temporal dispersion → acquired (CIDP)
- RNS rules: decrement >10% at 3 Hz → MG (postsynaptic); increment >60% on brief 10-sec exercise or 50 Hz rep stim → LEMS (presynaptic); botulism = increment but less dramatic
- SFEMG: increased jitter ± blocking is the MOST SENSITIVE test for NMJ disorders — but NOT specific (also abnormal in reinnervation)
- Myotonic discharge waveform: “dive bomber” waxing-waning AMPLITUDE AND FREQUENCY → myotonia congenita, paramyotonia, DM1/DM2, hyperkalemic PP, Pompe, IBM
- Temperature pitfall: cold limb increases CMAP amplitude AND prolongs latencies/slows CV — mimics demyelination; always warm to ≥32°C
- Distal-only stim error: CMT1A may look axonal if you only stim distally — MUST stimulate proximally to unmask uniform slowing
- Albuminocytologic dissociation: elevated CSF protein with normal WBC count → GBS and CIDP (supports demyelinating NCS pattern)
🔍 Buzzwords & Pathognomonic FindingsNCS patterns · EMG signal patterns · Disease associations
NCS patterns
- Conduction block at non-entrapment site → MMN or CIDP/AIDP (acquired demyelination)
- Temporal dispersion (CIDP > AIDP) → acquired demyelinating neuropathy
- Uniform symmetric slowing of CV → CMT1A (hereditary demyelinating)
- Multifocal slowing + conduction block → CIDP (acquired)
- Reduced CMAP/SNAP amplitudes, preserved CV → axonal neuropathy
- >60% increment on brief exercise / 50 Hz rep stim → LEMS (presynaptic NMJ)
- >10% decrement on 3 Hz rep stim → MG (postsynaptic NMJ)
- Increased jitter on single-fiber EMG → NMJ disorder (most sensitive)
EMG signal patterns
- Fibrillations + positive sharp waves → active denervation (2–3 wk after axonal injury) OR active myopathy with membrane instability
- Complex repetitive discharges (CRDs) → chronic denervation, dystrophies
- “Dive bomber” waxing-waning discharges → myotonic discharges (DM1/DM2, myotonia congenita, paramyotonia, Pompe, IBM)
- “Marching soldiers” continuous rippling → myokymia (radiation plexopathy, MS, Isaacs/CASPR2, snake bite)
- Continuous high-frequency motor unit firing → neuromyotonia (Isaacs/CASPR2, hereditary)
- Large, long-duration, polyphasic MUAPs + reduced recruitment → neurogenic (chronic reinnervation)
- Small, short-duration, polyphasic MUAPs + early recruitment → myopathic
- Gigantic motor units → post-polio, chronic ALS, Kennedy disease
Disease-specific signatures
- Diffuse continuous fasciculations + neurogenic MUAPs in 3 regions → ALS
- Tongue fasciculations (uncommon — suggests pathologic) → ALS, Kennedy disease
- Benign fasciculations → regular, brief, NO other EMG findings, no weakness
- Pure motor conduction block, asymmetric, upper limb predominant → MMN (anti-GM1)
- Albuminocytologic dissociation + demyelinating NCS >8 wk → CIDP
- Albuminocytologic dissociation + acute demyelinating NCS <4 wk → AIDP (GBS)
- Prolonged/absent F-wave with normal distal CV → early GBS (proximal demyelination)
- Absent H-reflex → S1 radiculopathy, polyneuropathy, GBS (early)
Nerve Conduction Study Basics
Motor NCS
- Technique: stimulate peripheral nerve → record CMAP from muscle via surface electrodes
- CMAP amplitude: reflects number of functioning motor axons (axonal integrity)
- Distal latency: time from distal stimulation to CMAP onset; prolonged in distal demyelination
- Conduction velocity: distance ÷ (proximal latency − distal latency); reflects myelination status
- F-wave: late response from antidromic activation of anterior horn cells → orthodromic return; tests entire motor nerve length including proximal segments; only ~1–5% of motor neurons backfire per stimulus, explaining variable latency/amplitude
Sensory NCS
- SNAP amplitude: reflects number of functioning sensory axons
- Sensory conduction velocity: reflects sensory nerve myelination
- Sensory NCS are normal in lesions proximal to DRG (radiculopathy, motor neuron disease)
Axonal vs Demyelinating Patterns
| Parameter | Axonal | Demyelinating |
|---|---|---|
| CMAP amplitude | Reduced (primary abnormality) | Reduced late (secondary axonal loss) or preserved early |
| SNAP amplitude | Reduced | May be preserved early |
| Conduction velocity | Normal or mildly slow (>70% LLN) | Significantly slow (<70% LLN) |
| Distal latency | Normal or mildly prolonged | Prolonged (>130% ULN) |
| Conduction block | Absent | Present (acquired demyelination) |
| Temporal dispersion | Absent | Present |
| F-wave latency | Normal or absent (severe axonal loss) | Prolonged or absent |
F-Waves & H-Reflex
| Late Response | Mechanism | Clinical Use | Key Points |
|---|---|---|---|
| F-wave | Antidromic activation of anterior horn cell → orthodromic return; NOT a reflex (no synapse) | Tests proximal nerve conduction; GBS, radiculopathy | Variable shape and latency; prolonged or absent in early GBS (often first abnormality) |
| H-reflex | Electrical equivalent of monosynaptic stretch reflex (Achilles reflex); elicited by submaximal tibial nerve stimulation, recorded from soleus/gastrocnemius; afferent Ia → S1 anterior horn → efferent motor | S1 radiculopathy; early GBS; polyneuropathy | Absent or prolonged H-reflex = S1 root or proximal sensory nerve involvement; one of first abnormalities in GBS |
💎 Board Pearl
- F-wave is NOT a reflex — it involves no synapse; it is a backfiring of the motor neuron; variable amplitude and latency with each stimulation
- In early GBS, F-waves and H-reflexes may be the ONLY abnormalities before distal NCS become abnormal
- Axonal neuropathy: amplitude drops proportionally to axon loss; velocity stays >70% LLN because surviving axons conduct normally
Conduction Block & Temporal Dispersion
Definitions
| Finding | Definition | Significance |
|---|---|---|
| Conduction block | >50% CMAP amplitude/area drop = definite conduction block (EFNS/PNS 2021); >30% drop = possible conduction block when combined with other demyelinating features | Acquired demyelination — CIDP, MMN, GBS; motor deficit without atrophy (early) |
| Temporal dispersion | >30% increase in CMAP duration between distal and proximal stimulation | Differential slowing of individual nerve fibers; acquired demyelinating neuropathies |
| Pseudo-conduction block | Up to 20% amplitude drop is normal across most segments; up to 25% across the elbow (ulnar) is acceptable | Submaximal stimulation, phase cancellation, or normal anatomic variation — NOT true demyelination |
Conduction Block — Disease Correlations
| Disease | Conduction Block? | Key Feature |
|---|---|---|
| CIDP | Yes — multifocal, motor and sensory nerves | Nonuniform slowing; symmetric; responds to IVIg/PE/steroids |
| MMN | Yes — motor nerves ONLY | Sensory NCS normal in same distribution; anti-GM1 Ab in ~50%; NO response to steroids |
| GBS (AIDP) | Yes — evolves over days to weeks | Sural sparing pattern; prolonged F-waves early |
| CMT1 | No — uniform slowing without block | Hereditary = uniform slowing to <38 m/s in upper limb motor nerves (Harding-Thomas criterion for CMT1A); often <20 m/s in severe cases; NO conduction block (distinguishes from CIDP) |
| Focal compressive neuropathy | Yes — at compression site only | Carpal tunnel, ulnar at elbow, peroneal at fibular head |
💎 Board Pearl
- Conduction block = acquired demyelination — if you see conduction block, think CIDP, MMN, or GBS; NEVER CMT1 (hereditary = uniform slowing, no block)
- MMN mimics ALS clinically (asymmetric LMN weakness) but EMG shows conduction block in motor nerves with normal sensory — MUST check before diagnosing ALS
- Conduction block causes weakness without atrophy (axon is intact but signal cannot pass) — atrophy develops only if secondary axonal loss occurs
Needle EMG Findings
Insertional & Spontaneous Activity
| Finding | Sound / Appearance | Significance |
|---|---|---|
| Normal insertional activity | Brief burst of activity with needle movement | Normal muscle; ceases when needle stops moving |
| Increased insertional activity | Prolonged electrical activity after needle movement | Early denervation, inflammatory myopathy, acute processes |
| Decreased insertional activity | Little or no activity with needle movement | Fibrosis, severe atrophy, fatty replacement (end-stage disease) |
Spontaneous Activity
| Discharge Type | Description | Associated Conditions |
|---|---|---|
| Fibrillation potentials | Single muscle fiber discharges; regular firing; small amplitude (20–300 μV typical range) | Denervation (2–3 weeks after injury), inflammatory myopathy, necrotizing myopathy, acid maltase deficiency |
| Positive sharp waves (PSWs) | Initial sharp positive deflection; same significance as fibrillations | Same as fibrillations — seen together; appear 2–3 weeks after denervation |
| Fasciculation potentials | Whole motor unit discharge; irregular firing; visible twitch under skin | ALS (most concerning), radiculopathy, benign fasciculations, thyrotoxicosis, anticholinesterase toxicity |
| Myotonic discharges | Waxing/waning amplitude AND frequency; “dive bomber” sound | DM1, DM2, myotonia congenita, paramyotonia congenita, acid maltase deficiency, hyperkalemic periodic paralysis |
| Complex repetitive discharges (CRDs) | “Machine-like” repetitive discharge; abrupt onset/offset; uniform frequency | Chronic denervation, chronic myopathy — nonspecific; polio, radiculopathy, muscular dystrophy |
| Myokymic discharges | Grouped repetitive bursts; “marching soldiers” sound | Radiation plexopathy (#1 association), GBS, MS (facial myokymia), timber rattlesnake envenomation |
| Neuromyotonic discharges | Very high frequency (150–300 Hz); decrementing amplitude; “pinging” sound | Isaacs syndrome (neuromyotonia), CASPR2/LGI1 antibodies, Morvan syndrome |
🎯 Clinical Pearl
- Myokymic discharges on EMG + history of radiation therapy = radiation plexopathy (not tumor recurrence); tumor recurrence typically shows fibrillations without myokymia
- Myotonic discharges have the classic “dive bomber” sound — if you hear waxing AND waning of BOTH amplitude and frequency, it is myotonia regardless of the clinical picture
Motor Unit Action Potentials (MUAPs)
| Parameter | Neurogenic | Myopathic |
|---|---|---|
| Amplitude | Large (increased due to reinnervation) | Small (fewer functioning muscle fibers per motor unit) |
| Duration | Long | Short |
| Phases | Polyphasic (may be) | Polyphasic (common) |
| Recruitment | Reduced (fewer motor units → increased firing rate of remaining units) | Early/rapid (all motor units fire but each generates less force) |
| Firing rate at recruitment | Fast (>15–20 Hz before new unit recruited) | Normal (<15 Hz); many units fire at low force levels |
| Interference pattern | Reduced (discrete or single-unit pattern in severe cases) | Full but at low force; “early recruitment” |
| Mechanism | Loss of motor neurons → surviving neurons reinnervate orphaned fibers → larger motor units | Loss of individual muscle fibers → smaller motor units with fewer fibers per unit |
💎 Board Pearl
- Reduced recruitment + large MUAPs = neurogenic; early recruitment + small MUAPs = myopathic — this is the single most important EMG distinction on boards
- Polyphasic MUAPs are nonspecific — seen in BOTH neurogenic and myopathic processes; up to 25% in deltoid; up to 15% in most limb muscles is normal
- In acute denervation (<3 weeks), MUAPs may appear normal because reinnervation has not yet occurred — fibrillations may be the only finding
Repetitive Nerve Stimulation (RNS)
Low-Frequency RNS (2–3 Hz)
- Principle: repeated stimulation depletes presynaptic ACh quanta; if NMJ safety factor is reduced, EPP falls below threshold → CMAP decrement
- Normal: no significant decrement (<10%)
- Abnormal decrement: ≥10% between 1st and 4th/5th response (U-shaped pattern: biggest drop at 3rd–4th stimulus, then partial repair)
- Most sensitive muscles: proximal — trapezius, deltoid, facial (nasalis); distal muscles less sensitive
- Post-exercise facilitation: 10 seconds of maximal exercise → temporary improvement (brief exercise transiently increases presynaptic ACh release, partially repairing the decrement in MG); test immediately after exercise
- Post-exercise exhaustion: worsened decrement at 2, 3, and 4 minutes after 1 minute of sustained maximal exercise
High-Frequency RNS (20–50 Hz)
- Principle: rapid stimulation causes massive Ca2+ accumulation at presynaptic terminal → increased ACh release
- LEMS: ≥60% increment in CMAP amplitude (AANEM current standard; historical threshold was 100%) — highly characteristic (diagnostic in appropriate clinical context)
- Botulism: facilitation present (similar to LEMS) but typically less dramatic (>60% increment)
- Note: high-frequency RNS is painful; can substitute brief maximal voluntary exercise (10 seconds) then recheck CMAP at rest
RNS Findings by NMJ Disorder
| Feature | MG | LEMS | Botulism |
|---|---|---|---|
| NMJ defect | Postsynaptic (AChR) | Presynaptic (VGCC) | Presynaptic (SNARE) |
| Baseline CMAP | Normal | Low amplitude | Low amplitude |
| Low-rate RNS (2–3 Hz) | ≥10% decrement | Decrement present | Decrement may be present |
| High-rate RNS (20–50 Hz) | No significant increment | ≥60% increment (AANEM current standard; historical threshold was 100%) — highly characteristic | Increment present (less dramatic) |
| Post-exercise facilitation | Brief repair of decrement (seconds) | Dramatic CMAP amplitude increase | Moderate CMAP amplitude increase |
| Sensory NCS | Normal | Normal | Normal |
| Needle EMG | Usually normal; unstable MUAPs (moment-to-moment variation) | Short-duration, low-amplitude MUAPs; may mimic myopathy | Short-duration MUAPs; fibrillations (in severe cases) |
💎 Board Pearl
- LEMS triad on electrodiagnostics: (1) low baseline CMAP, (2) decrement on low-rate RNS, (3) ≥60% increment on high-rate RNS or post-exercise (AANEM current standard; historical threshold was 100%) — diagnostic in appropriate clinical context
- In MG, RNS sensitivity is ~75% in generalized and ~30–50% in ocular MG — a normal RNS does NOT rule out MG (get SFEMG)
- AChE inhibitors (pyridostigmine) should be held ≥12 hours before RNS to avoid masking decrement
Single Fiber EMG (SFEMG)
Principles & Technique
| Feature | Details |
|---|---|
| What it measures | Jitter = variability in time interval between two single muscle fiber APs belonging to the same motor unit |
| Normal jitter | Normal mean MCD varies by muscle and age — e.g., EDC ~34 μs upper limit in voluntary SFEMG; values must be referenced against age- and muscle-specific norms |
| Blocking | Intermittent failure of one fiber to fire — indicates severe NMJ transmission failure |
| Sensitivity for MG | ~95% for generalized MG; ~90% for ocular MG (when clinically weak muscle tested) — most sensitive test for NMJ disorders |
| Specificity | Low — abnormal in ANY condition affecting NMJ transmission or fiber density |
| Stimulated SFEMG | Easier, more reproducible, no need for patient cooperation; uses nerve stimulation instead of voluntary activation |
Causes of Increased Jitter
| Category | Examples |
|---|---|
| NMJ disorders | MG (most sensitive test), LEMS, botulism, congenital myasthenic syndromes |
| Neurogenic (reinnervation) | ALS, radiculopathy, neuropathy — newly formed NMJs have immature, unstable transmission |
| Myopathic | Inflammatory myopathy, some muscular dystrophies — muscle fiber splitting creates new NMJs |
💎 Board Pearl
- SFEMG is the MOST SENSITIVE test for MG (~95% for generalized MG; ~90% for ocular MG when clinically weak muscle tested) but NOT the most specific — increased jitter is also seen in reinnervation (ALS, neuropathy) and myopathies
- A normal SFEMG in a clinically weak muscle essentially rules out MG in that muscle
- Test a clinically affected muscle for highest yield; extensor digitorum communis is the most commonly tested muscle
Pattern Recognition — NCS/EMG by Disease
Master Reference Table
| Disease | Motor NCS | Sensory NCS | Needle EMG | Key Finding |
|---|---|---|---|---|
| ALS | Reduced CMAP; normal velocities | Normal (hallmark) | Widespread fibs/PSWs + fasciculations; large neurogenic MUAPs with reduced recruitment | Diffuse denervation/reinnervation in ≥3 body regions (bulbar, cervical, thoracic, lumbosacral) with normal sensory |
| GBS (AIDP) | Prolonged DL, prolonged/absent F-waves, conduction block, temporal dispersion, slowed CV | Sural sparing pattern (normal sural, abnormal upper limb SNAPs) | Fibrillations (late, 2–3 weeks); reduced recruitment early | Sural sparing pattern; conduction block and temporal dispersion may be delayed (1–2 weeks); F-wave/H-reflex abnormalities are typically the earliest findings; evolves over days |
| CIDP | Same as AIDP but chronic; nonuniform slowing; conduction block; prolonged DL/F-waves | Reduced SNAPs | Chronic denervation/reinnervation; CRDs in longstanding cases | Nonuniform slowing differentiates from CMT1; conduction block present (unlike CMT1) |
| CMT1 | Uniform slowing ALL nerves (<38 m/s in upper limb motor nerves [Harding-Thomas criterion for CMT1A]; often <20 m/s in severe cases); no conduction block | Reduced or absent SNAPs | Chronic neurogenic changes | Uniform slowing + absent conduction block = hereditary; biopsy → onion bulbs |
| CMT2 | Reduced CMAP amplitudes; normal/near-normal velocities | Reduced SNAP amplitudes | Chronic neurogenic changes | Axonal pattern (reduced amplitudes, preserved velocities); distinguish from CMT1 by normal CV |
| MG | Normal CMAP at rest | Normal | Usually normal; unstable MUAPs; SFEMG → increased jitter | ≥10% decrement on low-rate RNS; SFEMG most sensitive (~95% generalized MG; ~90% ocular MG) |
| LEMS | Low CMAP at rest; ≥60% increment on high-rate RNS or post-exercise (AANEM current standard; historical threshold was 100%) | Normal | Short-duration, low-amplitude MUAPs (can mimic myopathy) | Low baseline CMAP + dramatic facilitation (≥60%) = highly characteristic (diagnostic in appropriate clinical context) |
| Myopathy (general) | Normal (or mildly reduced CMAP in severe) | Normal | Small, short, polyphasic MUAPs; early recruitment; ± fibrillations (if inflammatory/necrotizing) | Normal NCS + myopathic MUAPs; fibrillations suggest active/inflammatory process |
| Myotonic dystrophy | Normal or mildly reduced CMAP | Normal | Myotonic discharges (“dive bomber”); myopathic MUAPs | Myotonic discharges + myopathic MUAPs; DM1 > DM2 for EMG abnormalities |
| CIP (critical illness polyneuropathy) | Reduced CMAP amplitudes | Reduced SNAP amplitudes | Fibrillations; neurogenic MUAPs | Both CMAP AND SNAP reduced (axonal sensorimotor); ICU setting |
| CIM (critical illness myopathy) | Reduced CMAP amplitudes | Normal (key differentiator from CIP) | Fibrillations; myopathic MUAPs; reduced CMAP on direct muscle stimulation | Reduced CMAP + normal SNAP differentiates from CIP; direct muscle stimulation is confirmatory |
| MMN | Conduction block in motor nerves | Normal in same nerve distribution | Neurogenic changes in affected muscles; fasciculations may be present | Motor conduction block + normal sensory in same nerve = MMN (NOT ALS); anti-GM1 in ~50% |
| Radiculopathy | Normal (or reduced CMAP if severe/chronic) | Normal (lesion proximal to DRG) | Fibrillations in myotomal distribution + paraspinals; neurogenic MUAPs in chronic | Normal SNAP is KEY — lesion is at root level (proximal to DRG); paraspinal fibrillations localize to root |
🎯 Clinical Pearl
- CIP vs CIM: both present as ICU weakness with fibrillations; SNAP reduction differentiates (reduced in CIP, normal in CIM); direct muscle stimulation is low in CIM but normal in CIP
- MMN vs ALS: both cause asymmetric LMN weakness and fasciculations; conduction block with normal sensory NCS in the same nerve = MMN; treat with IVIg (NOT steroids, which worsen MMN)
Localization Principles
Electrodiagnostic Localization Algorithm
| Finding | Localization | Explanation |
|---|---|---|
| Paraspinal fibrillations | Root level | Paraspinal muscles innervated by posterior rami; NOT involved in plexus or peripheral nerve lesions |
| Reduced SNAP | Lesion distal to DRG (plexus or nerve) | DRG cell body is in the foramen; root avulsion leaves DRG intact → normal SNAP; plexus lesion damages axon distal to DRG → abnormal SNAP |
| Normal SNAP + abnormal CMAP | Motor neuron, root, NMJ, or muscle | Sensory axons unaffected (lesion proximal to DRG or affects only motor pathway) |
| Conduction block at specific site | Focal nerve lesion at that site | Carpal tunnel (median at wrist), cubital tunnel (ulnar at elbow), peroneal at fibular head |
| Diffuse slowing (<70% LLN) | Demyelinating neuropathy | Nonuniform = acquired (CIDP); uniform = hereditary (CMT1) |
| Normal NCS + abnormal SFEMG | NMJ disorder | MG, LEMS, congenital myasthenic syndromes |
| Myopathic MUAPs + normal NCS | Myopathy | Small short polyphasic MUAPs with early recruitment |
| Fibrillations in 2+ limbs across multiple root levels + fasciculations | Motor neuron disease (ALS) | Awaji — denervation evidence required in ≥2 regions combined with clinical UMN findings; ≥3 regions strengthens diagnostic certainty; SNAP must be normal |
Root vs Plexus vs Nerve
| Feature | Root (Radiculopathy) | Plexus (Plexopathy) | Peripheral Nerve |
|---|---|---|---|
| SNAP | Normal (lesion proximal to DRG) | Reduced (lesion distal to DRG) | Reduced (lesion distal to DRG) |
| CMAP | Normal or reduced (if severe) | Reduced | Reduced |
| Paraspinal fibs | Present | Absent | Absent |
| Distribution of EMG abnormalities | Single myotome, multiple nerves | Multiple nerves, multiple myotomes (trunk/cord pattern) | Single nerve distribution |
| Conduction velocity | Normal | Normal or mildly slow | Slow across lesion site |
💎 Board Pearl
- Normal SNAP = root level (the #1 electrodiagnostic rule for localization); reduced SNAP = plexus or peripheral nerve
- Paraspinal fibrillations confirm root-level pathology — plexus and nerve lesions do NOT produce paraspinal findings
- In preganglionic brachial plexus avulsion, SNAP is normal despite complete sensory loss clinically — because the DRG and its peripheral process are intact
- For ALS diagnosis: widespread denervation/reinnervation across multiple myotomes + normal sensory NCS + fasciculations — Awaji criteria allow fasciculation potentials to serve as evidence of denervation
Common EMG Pitfalls & Board Traps
High-Yield Pitfalls Table
| Pitfall | What Happens | Board-Relevant Point |
|---|---|---|
| Cold temperature | Slowed velocities, prolonged distal latencies, increased CMAP amplitude, increased SNAP amplitude | Can mimic demyelinating neuropathy; ALWAYS warm limb to ≥32°C before testing; most common technical error on boards |
| Martin-Gruber anastomosis | Motor axons cross from median to ulnar nerve in forearm; median CMAP larger at elbow than wrist (initial positive deflection at wrist) | Present in 15–30% of population; creates apparent conduction block or initial positive deflection; can confound carpal tunnel diagnosis |
| Submaximal stimulation | Not all axons activated → artificially low CMAP amplitude | Can falsely mimic conduction block; must use supramaximal stimulation (20% above maximal) |
| Wallerian degeneration timeline | NCS changes delayed: motor axons → 3–5 days; sensory axons → 7–11 days | EMG done <7 days after acute injury may appear normal; fibrillations take 2–3 weeks to appear; must wait for accurate assessment |
| Volume conduction | Recording electrode picks up signal from nearby muscles, not the target | Can produce initial positive deflection or unusually large CMAPs; verify proper electrode placement |
| Fibrillations in myopathy | Fibrillations are NOT exclusive to denervation — seen in inflammatory, necrotizing, and some dystrophies | Do NOT assume fibrillations = neurogenic; context matters — fibrillations + myopathic MUAPs = myopathy with active fiber necrosis |
| Sural sparing pattern | Normal sural SNAP with abnormal median/ulnar SNAPs | Classic for GBS (AIDP) — distal demyelination preferentially affects upper limb sensory nerves; highly specific for GBS in acute weakness setting |
| Inching (short-segment studies) | Stimulation at 1–2 cm increments across suspected lesion site | Precisely localizes focal conduction block or slowing; useful for ulnar neuropathy at elbow, carpal tunnel syndrome |
| Accessory peroneal nerve | Anomalous innervation of EDB from behind lateral malleolus (branch of superficial peroneal) | Ankle CMAP is smaller than below-fibular-head CMAP; stimulate behind lateral malleolus to identify; present in ~20% of population |
| Median-ulnar crossover (Riche-Cannieu) | Ulnar motor fibers cross to median in the hand, innervating thenar muscles | All hand muscles may be ulnar-innervated in extreme cases; affects interpretation of median motor studies |
💎 Board Pearl
- Temperature is the #1 technical pitfall: cold hand = slow velocities + high amplitudes = false demyelination; warm to ≥32°C (hand) / ≥34°C (leg)
- Martin-Gruber anastomosis: if median CMAP at elbow is > CMAP at wrist, suspect anomalous crossover, not conduction block; stimulate ulnar at wrist to confirm
- Sural sparing pattern: normal sural + abnormal upper limb SNAPs in acute weakness = GBS until proven otherwise
- Timing matters: do NOT perform EMG/NCS <2 weeks after acute injury if looking for fibrillations; motor NCS can be done >5 days for axonal loss documentation
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