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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 (<75% LLN), prolonged distal latencies, conduction block, temporal dispersion
Conduction block = acquired demyelination: >50% CMAP amplitude drop between distal and proximal stimulation; 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 = >100% increment at 20–50 Hz (presynaptic); botulism = increment (less dramatic than LEMS)
SFEMG: most sensitive test for NMJ disorders (95–99% for MG); 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

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

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 (>75% LLN)	Significantly slow (<75% 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); 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 >75% LLN because surviving axons conduct normally

Conduction Block & Temporal Dispersion

Definitions

Finding	Definition	Significance
Conduction block	>50% drop in CMAP amplitude (or area) between distal and proximal stimulation sites; >30% for tibial/peroneal nerves	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 <25 m/s in all nerves; 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 (20–200 μV)	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 15% polyphasic MUAPs 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 (Ca²⁺ mobilization repairs decrement); test immediately after exercise
Post-exercise exhaustion: worsened decrement 2–4 minutes after sustained exercise

High-Frequency RNS (20–50 Hz)

Principle: rapid stimulation causes massive Ca²⁺ accumulation at presynaptic terminal → increased ACh release
LEMS: >100% increment in CMAP amplitude (dramatic facilitation) — pathognomonic
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	>100% increment (pathognomonic)	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) >100% increment on high-rate RNS or post-exercise — pathognomonic
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	<55 μsec for most muscles (varies by muscle and age)
Blocking	Intermittent failure of one fiber to fire — indicates severe NMJ transmission failure
Sensitivity for MG	95–99% (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 (95–99%) 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; F-wave prolongation is earliest finding; 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 (<25 m/s in upper limbs); 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 (95–99%)
LEMS	Low CMAP at rest; >100% increment on high-rate RNS or post-exercise	Normal	Short-duration, low-amplitude MUAPs (can mimic myopathy)	Low baseline CMAP + dramatic facilitation (>100%) = pathognomonic
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 (<75% 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)	Must involve ≥3 body regions (revised El Escorial / Awaji criteria); 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