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10 notes available
1 Last Minute Review 2 Polyneuropathies 3 Mononeuropathies & Plexopathies 4 Motor Neuron Disease 5 Myasthenia Gravis & NMJ Disorders 6 Inflammatory Myopathies 7 Muscular Dystrophies 8 Channelopathies & Metabolic Myopathies 9 Neuromuscular Emergencies 10 EMG/NCS Patterns
Clinical › Neuromuscular

EMG/NCS Patterns

EMG/NCS Patterns in Neuromuscular Disease

What You'll Learn

  • 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
HighYield Pearls
  • 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)
🔍 Quick ReferenceNCS 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
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