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NCS & EMG Basics

Physiology

⚡ NCS Basics

Motor vs Sensory NCS

Feature Motor NCS (CMAP) Sensory NCS (SNAP)
Recording site Muscle Sensory nerve (digit or nerve trunk)
Amplitude reflects Number of motor axons + muscle fibers Number of sensory axons
Normal amplitude >4-5 mV (varies by nerve) >10-20 ΞV (varies by nerve)
Key clinical use Motor axon loss, NMJ, myopathy Distinguishes pre- vs postganglionic lesions

Key NCS Parameters

Parameter What It Measures Abnormal In
Amplitude Number of functioning axons Axonal loss, conduction block
Conduction velocity (CV) Speed of fastest fibers (myelination) Demyelination (<70-75% LLN)
Distal latency (DL) Time from distal stim to response Distal demyelination (>130% ULN)
Duration Synchrony of fiber conduction Temporal dispersion (demyelination)
💎 Board Pearl

SNAP preserved in radiculopathy because the lesion is preganglionic (DRG intact). SNAP lost in plexopathy and peripheral neuropathy (postganglionic). This is key for localization!

🔍 Demyelinating vs Axonal Patterns

NCS Criteria

Feature Demyelinating Axonal
Conduction velocity <70-75% LLN Normal or mildly slow (>70% LLN)
Distal latency >130% ULN Normal or mildly prolonged
Amplitude May be preserved early; low late Low (proportional to axon loss)
Temporal dispersion Present (>30% duration increase) Absent
Conduction block Present (>50% amplitude drop) Absent
F-wave latency Prolonged or absent Normal or mildly prolonged
EMG fibrillations Less prominent (unless 2° axonal loss) Prominent

Clinical Examples

Demyelinating Axonal
GBS (AIDP) GBS (AMAN, AMSAN)
CIDP Diabetic polyneuropathy
CMT1 (hereditary) CMT2 (hereditary)
MMN Toxic neuropathies
Anti-MAG neuropathy Vasculitic neuropathy
💎 Board Pearl

Conduction block = weakness WITHOUT atrophy (axons intact but can’t conduct through demyelinated segment). Temporal dispersion indicates acquired (non-uniform) demyelination – not seen in hereditary demyelinating neuropathies like CMT1.

📍 NCS Patterns by Location

Common Mononeuropathies – Entrapment Sites

Nerve Site NCS Findings Clinical
Median Carpal tunnel Prolonged DL; slow sensory CV across wrist; compare to ulnar Numbness digits 1-3; thenar weakness (severe)
Ulnar Elbow (cubital tunnel) CV slowing across elbow (>10 m/s drop); conduction block Numbness digits 4-5; intrinsic hand weakness
Ulnar Wrist (Guyon’s canal) Abnormal dorsal ulnar cutaneous spares (branches proximal) Similar to elbow but dorsum hand spared
Peroneal Fibular head Conduction block/slowing across fibular head; superficial peroneal SNAP normal Foot drop; lateral leg numbness
Radial Spiral groove Conduction block across spiral groove Wrist drop; Saturday night palsy
Tibial Tarsal tunnel Prolonged DL; low amplitude medial/lateral plantar Sole numbness/burning

Radiculopathy vs Plexopathy vs Neuropathy

Feature Radiculopathy Plexopathy Mononeuropathy
SNAP Normal (preganglionic) Abnormal Abnormal
CMAP Low (if severe axon loss) Low Low
EMG distribution Myotomal (multiple nerves, one root) Multiple nerves/roots, one plexus region Single nerve distribution
Paraspinals Abnormal Normal Normal
💎 Board Pearl

SNAP normal + paraspinals abnormal = radiculopathy. SNAP abnormal + paraspinals normal = plexopathy or peripheral nerve lesion. This is the most important distinction!

🔎 Special NCS Studies

Late Responses

Study Pathway Clinical Use Abnormal In
F-wave Motor nerve → anterior horn → back (antidromic-orthodromic) Tests proximal nerve segments, roots GBS (early), radiculopathy, proximal neuropathy
H-reflex Ia afferent → spinal cord → motor neuron (monosynaptic) Electrical ankle jerk; tests S1 root S1 radiculopathy, polyneuropathy

Repetitive Nerve Stimulation (RNS)

Finding Low-Frequency (2-3 Hz) Post-Exercise/High-Frequency Diagnosis
Decrement >10% Yes Repair of decrement Myasthenia gravis
Low baseline + increment >100% May decrement Large increment Lambert-Eaton
Low baseline + small increment May decrement 20-40% increment Botulism

Blink Reflex

💎 Board Pearl

F-waves test the entire motor nerve including proximal segments – prolonged or absent early in GBS when distal NCS still normal. H-reflex = S1; absent H-reflex with normal ankle jerk suggests early/mild S1 radiculopathy.

📊 EMG Spontaneous Activity

Types of Spontaneous Activity

Finding Description Sound Associated Conditions
Fibrillation potentials Spontaneous single muscle fiber discharge; biphasic/triphasic; regular “Rain on a tin roof” Denervation, inflammatory myopathy, muscular dystrophy, NMJ disorders
Positive sharp waves (PSWs) Initial positive deflection then negative; regular Dull “thud” Same as fibrillations
Fasciculation potentials Spontaneous motor unit discharge; irregular “Popcorn” ALS, radiculopathy, benign fasciculations, cramp-fasciculation syndrome
Myotonic discharges Waxing and waning frequency AND amplitude; triggered by needle movement “Dive bomber” Myotonic dystrophy, myotonia congenita, paramyotonia, hyperkalemic PP
Myokymic discharges Grouped, repetitive bursts of same MUP; semi-rhythmic “Marching soldiers” Radiation plexopathy, GBS, MS, facial myokymia (brainstem glioma)
Neuromyotonic discharges Very high frequency (150-300 Hz); decrementing; “pinging” “Ping” or musical Isaac’s syndrome (anti-VGKC/CASPR2), thymoma, post-radiation
Complex repetitive discharges (CRDs) Polyphasic; regular; abrupt start/stop; no waxing/waning “Jackhammer” or “motorcycle” Chronic denervation, chronic myopathy, radiculopathy
Cramp potentials High-frequency MUP discharge; irregular; painful Rumbling Cramps (ALS, metabolic, benign)
💎 Board Pearl

Myotonic discharge = waxing/waning (dive bomber). CRD = NO waxing/waning (jackhammer). Myokymia on EMG = consider radiation injury or GBS. Neuromyotonia = Isaac’s syndrome (continuous muscle fiber activity).

⏱ïļ EMG in Denervation & Reinnervation

Timeline of EMG Changes After Nerve Injury

Time After Injury NCS Findings EMG Findings
Immediate (0-7 days) Conduction block at injury site; distal responses NORMAL Reduced recruitment only; NO fibrillations yet
Acute (7-10 days) Distal CMAP/SNAP drop (Wallerian degeneration complete) Reduced recruitment; fibs/PSWs starting (proximal muscles first)
Subacute (2-3 weeks) Low/absent distal responses Fibs/PSWs prominent in proximal muscles
Subacute (4-6 weeks) Low/absent distal responses Fibs/PSWs in distal muscles; maximal denervation
Early reinnervation (2-4 months) May see nascent CMAPs Nascent MUPs (small, polyphasic); fibs persist
Chronic reinnervation (6+ months) CMAP may improve Large, polyphasic MUPs; reduced recruitment; fibs decrease
Chronic stable (years) May be normal or low amplitude Giant MUPs; reduced recruitment; NO fibs (stable)

Key Points

💎 Board Pearl

Wait 3 weeks for optimal EMG after nerve injury – fibs take time to appear. Fibs WITHOUT large MUPs = acute/ongoing denervation. Fibs WITH large MUPs = chronic with ongoing denervation. Large MUPs WITHOUT fibs = chronic stable.

📈 MUP Analysis & Recruitment

Myopathic vs Neurogenic MUPs

Feature Myopathic Neurogenic
Amplitude Low (small) High (large/giant)
Duration Short Long
Phases Increased polyphasia Increased polyphasia
Recruitment Early (many small units for weak effort) Reduced (few units firing fast)
Reason Fewer muscle fibers per motor unit Collateral sprouting → larger motor units

Recruitment Patterns

Pattern Description Seen In
Normal Ratio ~5:1 (firing rate : number of MUPs) Normal
Reduced (neurogenic) Few MUPs firing rapidly (>15-20 Hz before next recruited) Neuropathy, radiculopathy, ALS
Early (myopathic) Many MUPs at low firing rates; full interference with weak effort Myopathy
Poor activation Few MUPs at low firing rates; normal MUP morphology UMN lesion, pain, poor effort
💎 Board Pearl

Myopathic = SNAP (Small, short, polyphasic with early recruitment). Neurogenic = LARP (Large amplitude, long duration, reduced recruitment, polyphasic). Remember: “Sick muscle = small units, sick nerve = big units.”

ðŸŽŊ Disease-Specific EMG Findings

Quick Recognition Table

Disease Key EMG/NCS Findings
ALS Widespread fibs + fasciculations + neurogenic MUPs; NORMAL sensory NCS; multiple regions (bulbar, cervical, thoracic, lumbar)
Myasthenia gravis Decrement on RNS; increased jitter on single-fiber EMG; normal routine NCS/EMG
Lambert-Eaton Low CMAP amplitude; >100% increment post-exercise; may have mild decrement at rest
GBS (AIDP) Prolonged/absent F-waves (early); conduction block; temporal dispersion; slow CV
CIDP Same as AIDP but symmetric and chronic; uniform demyelination
Multifocal motor neuropathy (MMN) Conduction block in motor nerves ONLY; normal sensory; asymmetric
Myotonic dystrophy Myotonic discharges (dive bomber); myopathic MUPs; fibs common
Polymyositis/Dermatomyositis Fibs/PSWs + myopathic MUPs (“irritable myopathy”); CRDs; normal NCS
Inclusion body myositis Mixed myopathic AND neurogenic features; fibs; long-duration MUPs
Steroid myopathy Myopathic MUPs; NO fibrillations; normal NCS
Critical illness myopathy Low CMAP with direct muscle stimulation; fibs; myopathic MUPs
Radiation plexopathy Myokymic discharges; axonal loss pattern
Isaac’s syndrome Neuromyotonic discharges; fasciculations; doublets/triplets
Carpal tunnel syndrome Prolonged median distal latency; slow sensory CV across wrist; compare to ulnar (normal)
💎 Board Pearl

ALS = motor only (normal sensory NCS is required). MMN = motor conduction block only. IBM = mixed pattern (unique!). Radiation plexopathy = myokymia (distinguishes from tumor infiltration which doesn’t have myokymia).

📋 Summary Tables

Localization Quick Reference

Clinical Scenario SNAP Paraspinals Diagnosis
Weakness + sensory loss in one nerve Abnormal Normal Mononeuropathy
Weakness in myotome + sensory loss in dermatome Normal Abnormal Radiculopathy
Weakness/sensory loss spanning multiple nerves and roots Abnormal Normal Plexopathy
Length-dependent sensory > motor Abnormal (distal) Normal Polyneuropathy

Spontaneous Activity Quick Reference

Sound Finding Think Of
“Dive bomber” (waxing/waning) Myotonic discharge Myotonic dystrophy, myotonia congenita
“Marching soldiers” (grouped bursts) Myokymia Radiation injury, GBS
“Ping” (high-frequency, decrementing) Neuromyotonia Isaac’s syndrome
“Jackhammer” (no waxing/waning) CRD Chronic denervation/myopathy
“Rain on tin roof” Fibrillations Denervation, inflammatory myopathy

Key Clinical Pearls

🔍 High-Yield Points
  • SNAP normal = preganglionic (radiculopathy)
  • Conduction block = demyelinating
  • Low amplitude everywhere = axonal
  • Wait 3 weeks for EMG after nerve injury
  • Fibs appear proximal to distal (paraspinals first)
  • Myopathic = small, short, early recruitment
  • Neurogenic = large, long, reduced recruitment
  • F-waves abnormal early in GBS (before distal changes)
  • Myokymia = radiation plexopathy
  • ALS requires normal sensory NCS

Red Flags

⚠ïļ Important Considerations
  • Fibs in first week: Pre-existing denervation or myopathy (not new injury)
  • Abnormal sensory NCS in suspected ALS: Reconsider diagnosis
  • Conduction block in sensory AND motor: Think CIDP/GBS, not MMN
  • Rapidly progressive with normal EMG: Consider NMJ disorder, myopathy, or too early after injury
  • Myokymia without radiation history: Consider GBS, MS, or brainstem lesion
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