🧠 Nerve/MuscleTool

Interactive EMG/NCS Case Studies

Learning Approach: Practice clinical reasoning with realistic cases. Each case follows the workflow: Patient Presentation → Physical Exam → Differential Building → NCS/EMG Results → Final Diagnosis.

Ready to test your EMG/NCS knowledge?

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⚡ Choose Your Challenge Level

Select which difficulty levels you want to practice with

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Beginner

Learning the Basics

ACTIVE

Perfect for residents starting their EMG/NCS journey

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Intermediate

Building Skills

ACTIVE

Ready for more complex diagnostic challenges

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Expert

Master Level

ACTIVE

Advanced cases that challenge even experts

📋 Patient Presentation

Key Principles for Differential Building

Location, Location, Location: Anatomical distribution is key
Time Course: Acute vs. chronic, progressive vs. stable
Associated Symptoms: Pain, sensory loss, weakness pattern
Pattern Recognition: Mononeuropathy, polyneuropathy, radiculopathy, myopathy
Risk Factors: Diabetes, trauma, repetitive motion, family history

Nerve Conduction Studies

Complete NCS Reference: Essential studies are highlighted with ⭐ ESSENTIAL badges - master these first. Advanced studies follow for complex cases. All studies from Preston & Shapiro included.

⚡ Key Technical Points - Cardinal Rules of NCS

🌡️ Temperature Control

Keep limbs warm (>32°C) - cold slows conduction velocity

⚡ Supramaximal Stimulation

Increase intensity until no further amplitude increase, then add 20%

🎯 Electrode Placement

Precise anatomical landmarks are crucial for reproducible results

📏 Distance Measurement

Use consistent surface measurements with tape measure

🔇 Artifact Minimization

Proper grounding and electrode impedance (<5 kΩ)

🎛️ Stimulator Optimization

Start with low intensity, find optimal position, then increase

Median Sensory

Recording: Index finger (digit 2) or middle finger (digit 3)

Stimulation: Wrist - between FCR tendon and palmaris longus tendon, 14 cm proximal to recording electrode

Anatomical Landmarks:
• Wrist: Between flexor carpi radialis (FCR) and palmaris longus tendons
• Feel for FCR tendon with wrist flexion and radial deviation
• Palmaris longus absent in ~15% of population

Normal Values:
• Amplitude: >15 μV
• Velocity: >50 m/s
• Peak Latency: <3.5 ms

Ulnar Sensory

Recording: Fifth digit

Stimulation: Wrist - just radial to FCU tendon, 14 cm proximal to recording electrode

Anatomical Landmarks:
• Wrist: Just radial (lateral) to flexor carpi ulnaris (FCU) tendon
• FCU tendon easily palpated with wrist flexion and ulnar deviation
• Nerve lies between FCU tendon and ulnar artery

Normal Values:
• Amplitude: >10 μV
• Velocity: >50 m/s
• Peak Latency: <3.5 ms

Dorsal Ulnar Cutaneous (DUC)

Recording: Dorsal hand between 4th and 5th metacarpals

Stimulation: Medial forearm, 10 cm proximal to ulnar styloid

Anatomical Landmarks:
• Stimulation: 10 cm proximal to ulnar styloid along medial forearm
• Between FCU and ulnar shaft
• DUC branches from main ulnar nerve ~5-8 cm proximal to wrist

Clinical Use:
• Differentiates ulnar neuropathy at wrist vs. elbow
• Normal in ulnar neuropathy at wrist

Radial Sensory

Recording: Dorsal web space between thumb and index finger

Stimulation: Lateral forearm between brachioradialis and ECRL tendons

Anatomical Landmarks:
• Stimulation: Between brachioradialis and extensor carpi radialis longus (ECRL)
• ~10 cm proximal to radial styloid
• Nerve becomes superficial at junction of middle and distal third of forearm

Normal Values:
• Amplitude: >15 μV
• Velocity: >50 m/s

Median Motor

Recording: Thenar muscles (APB)

Stimulation: Wrist, elbow

Anatomical Landmarks:
• Wrist: Between FCR and palmaris longus tendons
• Elbow: Medial to brachial artery, medial edge of biceps tendon
• In antecubital fossa, just medial to brachial artery pulsation

Normal Values:
• Distal Amplitude: >4 mV
• Distal Latency: <4.4 ms
• Velocity: >50 m/s

Ulnar Motor

Recording: Hypothenar muscles (ADM)

Stimulation: Wrist, below elbow, above elbow

Anatomical Landmarks:
• Wrist: Just radial to FCU tendon
• Below elbow: In cubital tunnel, between medial epicondyle and olecranon
• Above elbow: Medial arm, 10 cm above medial epicondyle
• Keep elbow flexed ~90° for below/above elbow stimulation

Normal Values:
• Distal Amplitude: >6 mV
• Distal Latency: <3.3 ms
• Velocity: >50 m/s

Fibular (Peroneal) Motor

Recording: Extensor digitorum brevis (EDB)

Stimulation: Ankle, fibular head, popliteal fossa

Anatomical Landmarks:
• Ankle: Lateral to extensor hallucis longus tendon, above ankle joint
• Fibular head: Just posterior and inferior to fibular head
• Popliteal fossa: Lateral edge, follow biceps femoris tendon
• Common fibular nerve wraps around fibular neck

Normal Values:
• Distal Amplitude: >2.5 mV
• Distal Latency: <6.5 ms
• Velocity: >44 m/s

Tibial Motor

Recording: Abductor hallucis

Stimulation: Ankle, popliteal fossa

Anatomical Landmarks:
• Ankle: Posterior to medial malleolus, between malleolus and Achilles tendon
• Popliteal fossa: Medial edge, between medial and lateral heads of gastrocnemius
• At ankle, nerve lies between flexor digitorum longus and flexor hallucis longus

Normal Values:
• Distal Amplitude: >4 mV
• Distal Latency: <5.8 ms
• Velocity: >41 m/s

Sural Sensory

Recording: Lateral foot behind lateral malleolus

Stimulation: Mid-calf, lateral to Achilles tendon, 14 cm proximal

Anatomical Landmarks:
• Recording: Behind and below lateral malleolus
• Stimulation: Mid-calf, lateral border of Achilles tendon
• Nerve lies between lateral border of Achilles and lateral malleolus

Clinical Use:
• Often preserved in L5/S1 radiculopathy
• Affected early in polyneuropathy

Median Sensory - Ring Finger (Mixed)

Recording: Ring finger (digit 4)

Stimulation: Wrist, 14 cm proximal

Purpose: Compares median vs ulnar innervation to ring finger
Normal: Median amplitude usually smaller than ulnar
Pathological significance: Median > ulnar suggests ulnar neuropathy

Median Sensory - Thumb

Recording: Thumb (digit 1)

Stimulation: Wrist, 10 cm proximal

Purpose: Pure median sensory territory
Technique: Bar electrodes on thumb
Clinical use: Carpal tunnel syndrome evaluation

Median Motor - 2nd Lumbrical

Recording: 2nd lumbrical muscle

Stimulation: Wrist

Electrode placement: Between 2nd and 3rd metacarpals
Purpose: Distal median motor function
Advantage: No ulnar innervation contamination

Ulnar Sensory - Little Finger

Recording: Little finger (digit 5)

Stimulation: Wrist, 14 cm proximal

Landmark: Just medial to FCU tendon
Purpose: Pure ulnar sensory territory
Normal values: Peak latency <3.7 ms, amplitude >6 μV

Ulnar Motor - First Dorsal Interosseous

Recording: First dorsal interosseous

Stimulation: Wrist, below elbow, above elbow

Electrode placement: Between thumb and index metacarpals
Purpose: Deep branch ulnar motor function
Clinical use: Ulnar neuropathy at Guyon's canal

Radial Sensory - Superficial Branch

Recording: Anatomical snuffbox

Stimulation: Forearm, 10-12 cm proximal

Landmark: Lateral border of radius
Purpose: Superficial radial nerve function
Clinical use: Radial tunnel syndrome, Saturday night palsy

Radial Motor - Extensor Indicis

Recording: Extensor indicis muscle

Stimulation: Posterior interosseous nerve at forearm

Electrode placement: Dorsal forearm, ulnar to EPL tendon
Purpose: Posterior interosseous nerve function
Clinical use: Radial tunnel syndrome

Lateral Antebrachial Cutaneous

Recording: Lateral forearm

Stimulation: Lateral elbow, 14 cm proximal

Purpose: Musculocutaneous nerve sensory branch
Clinical use: Lateral cord plexopathy
Technique: Patient supination, stimulate lateral to biceps

Medial Antebrachial Cutaneous

Recording: Medial forearm

Stimulation: Medial elbow, 14 cm proximal

Purpose: Medial cord function
Clinical use: Medial cord plexopathy, thoracic outlet syndrome
Normal: Often small amplitude, difficult to obtain

Median-Ulnar Comparison Studies

Multiple comparison techniques

Palmar mixed (palm-wrist): 8 cm segment
Ring finger comparison: Median vs ulnar to digit 4
Thumb-little finger: Median digit 1 vs ulnar digit 5
Purpose: Increase sensitivity for carpal tunnel syndrome
Normal: <0.4 ms difference median-ulnar latencies

Axillary Motor

Recording: Deltoid muscle (middle portion)

Stimulation: Erb's point

Electrode placement: Lateral deltoid, 10-12 cm from acromion
Purpose: Posterior cord/axillary nerve function
Clinical use: Shoulder trauma, quadrilateral space syndrome

Suprascapular Motor

Recording: Supraspinatus or infraspinatus

Stimulation: Suprascapular notch

Purpose: Upper trunk brachial plexus
Clinical use: Erb's palsy, suprascapular nerve entrapment
Technique: Needle electrodes often required

Long Thoracic Motor

Recording: Serratus anterior

Stimulation: Erb's point

Purpose: Long thoracic nerve function
Clinical use: Winged scapula, neuralgic amyotrophy
Technique: Patient in lateral position

Spinal Accessory Motor

Recording: Upper trapezius

Stimulation: Posterior border SCM muscle

Purpose: CN XI function
Clinical use: Neck surgery complications, trauma
Normal: Bilateral comparison important

Cardinal Rules of NCS (Preston & Shapiro)

Essential principles that every resident must remember:

NCS are an extension of the clinical examination - Always correlate findings with clinical symptoms
When in doubt, think technical factors - Most "abnormalities" are technical errors
When in doubt, reexamine the patient - If findings don't match exam, recheck both
Use supramaximal stimulation - Increase current 20% beyond plateau
Optimize stimulator position - Find lowest threshold, then increase to supramaximal
Don't overcall abnormalities - Minor findings without clinical correlation may be irrelevant

Key Technical Points

Temperature: Keep limbs warm (>32°C) - cold slows conduction velocity
Supramaximal Stimulation: Increase intensity until no further amplitude increase, then add 20%
Electrode Placement: Precise anatomical landmarks are crucial for reproducible results
Distance Measurement: Use consistent surface measurements with tape measure
Artifact Minimization: Proper grounding and electrode impedance (<5 kΩ)
Stimulator Optimization: Start with low intensity, find optimal position, then increase

Volume Conduction Principles

Understanding how electrical signals travel from nerve/muscle to recording electrodes:

Near-field Potentials: Most NCS record near-field potentials (CMAPs, SNAPs)
Triphasic Waveforms: Advancing action potential creates positive→negative→positive phases
Biphasic Waveforms: Action potential starting under electrode (motor studies)
Distance Effects: Amplitude decreases with distance from source
Far-field Potentials: Stimulus artifact is example - appears instantly at all sites

Temporal Dispersion & Phase Cancellation

Why proximal sensory responses are smaller and longer:

Temporal Dispersion: Fast fibers arrive before slow fibers (more with distance)
Phase Cancellation: Positive phase of fast fibers overlaps negative phase of slow fibers
Normal Effect: Proximal SNAPs have lower amplitude, longer duration
Pathological Enhancement: Demyelination worsens these effects
Motor vs Sensory: Less prominent in motor studies due to longer MUAP duration

Orthodromic vs Antidromic Studies

Two methods for sensory conduction studies:

Antidromic (Preferred):
• Stimulate nerve, record from digit
• Higher amplitude responses
• May have volume-conducted motor potential
• Better for small/pathologic potentials

Orthodromic:
• Stimulate digit, record from nerve
• Lower amplitude responses
• No motor contamination
• Useful when antidromic unclear
• Same latencies as antidromic

Basic Nerve Physiology for NCS

Understanding saltatory conduction and myelination:

Myelinated Fibers: Conduct 35-75 m/s via saltatory conduction
Nodes of Ranvier: Action potential "jumps" between nodes (every ~1mm)
Unmyelinated Fibers: Conduct 0.2-1.5 m/s (pain, temperature, autonomic)
Myelin Function: Insulates internodes, reduces capacitance, speeds conduction
NCS Records: Only largest, fastest myelinated fibers

Nerve Fiber Classification (Preston & Shapiro)

Motor Fibers:
• Aα (6-12 μm diameter, 35-75 m/s)
• Recorded in routine motor NCS

Sensory Fibers:
• Aβ (6-12 μm, 35-75 m/s) - Touch, vibration, recorded in routine sensory NCS
• Aδ (1-5 μm, 5-30 m/s) - Pain, temperature, NOT recorded in routine NCS
• C fibers (0.2-1.5 μm, 1-2 m/s) - Pain, temperature, NOT recorded

Muscle Afferents (Ia fibers):
• Aα (12-21 μm, 80-120 m/s) - Largest, fastest fibers
• Only recorded in mixed nerve studies
• Often first affected in demyelinating lesions

Mixed Nerve Studies

When and why to use mixed nerve studies:

Records All Fibers: Motor, sensory, AND muscle afferents (Ia fibers)
Fastest Velocities: Include largest Ia fibers (up to 120 m/s)
Early Demyelination: Ia fibers affected first in entrapment neuropathies
Common Studies: Median palm-wrist, ulnar palm-wrist, tibial across tarsal tunnel
Technique: Similar to sensory studies but records all nerve fibers

Wallerian Degeneration Timeline

Critical timing for interpreting acute nerve injuries:

Day 0-3: Normal distal NCS despite proximal nerve injury
Day 3-5: Motor responses begin to decline
Day 6-10: Sensory responses begin to decline
Day 7-10: Distal nerve becomes inexcitable
Weeks 2-3: Fibrillations appear on needle EMG
Months 3-6: Reinnervation potentials appear if recovery occurs

Clinical Implication: Normal NCS in first week don't exclude severe nerve injury

EMG Machine Components & Needles

Amplifier

Amplifies the small electrical signals from muscles and nerves (typically 1000-10,000 times amplification).

Key Features:
• High input impedance
• Low noise
• Differential amplification

Filters

Remove unwanted frequencies and noise from the signal.

Settings:
• Low-frequency filter: 2-10 Hz
• High-frequency filter: 10-10,000 Hz
• Notch filter: 60 Hz (removes power line noise)

Stimulator

Delivers electrical pulses to stimulate nerves during NCS.

Parameters:
• Duration: 0.1-1.0 ms
• Intensity: 0-300 mA
• Can deliver single or repetitive pulses

Display Monitor

Shows the amplified and processed electrical signals in real-time.

Display Options:
• Waveform visualization
• Multiple trace overlay
• Measurement cursors
• Real-time parameter calculation

Audio System

Converts electrical signals to sound for EMG needle examination.

Importance:
• Helps identify abnormal spontaneous activity
• Assists in motor unit analysis
• Provides real-time feedback during needle insertion

Ground Electrode

Provides electrical reference point and reduces artifact.

Placement:
• Between stimulator and recording electrodes
• Over bony prominence
• Must have good skin contact

EMG Needle Types

Monopolar Needle

Single recording surface at the tip with reference electrode on the skin.

Characteristics:
• Large recording area
• Higher amplitude signals
• More painful insertion
• Better for detecting small potentials

Concentric Needle

Central wire surrounded by cannula; most commonly used needle.

Characteristics:
• Smaller recording area
• Less painful
• Better spatial resolution
• More selective recording

Single Fiber Needle

Extremely small recording surface for specialized studies.

Uses:
• Single fiber EMG
• Neuromuscular junction disorders
• Requires special expertise
• Not used in routine EMG

Safety Note: Always use sterile, disposable needles. Follow universal precautions and proper needle disposal protocols.

Essential EMG Terminology

Insertional Activity

Brief electrical activity that occurs when the needle is inserted or moved within the muscle. Normal duration is less than 300ms. Increased insertional activity may indicate muscle membrane instability.

Spontaneous Activity

Electrical activity present in muscle at rest after insertional activity has ceased. Normal muscle is electrically silent at rest. Abnormal spontaneous activity includes fibrillations, positive sharp waves, and fasciculations.

Fibrillation Potentials

Small amplitude (20-200 μV), short duration (1-5 ms) potentials that fire regularly at 1-50 Hz. Sound like "rain on a tin roof." Indicate denervated muscle fibers, typically appearing 2-3 weeks after nerve injury.

Positive Sharp Waves

Initially positive, sharp deflection followed by slow negative phase. Similar significance to fibrillation potentials but represent different firing patterns of denervated muscle fibers. Sound like "dull thuds."

Fasciculations

Spontaneous firing of an entire motor unit, producing larger amplitude potentials than fibrillations. Can be benign or pathological. Often visible through the skin as muscle twitching.

Motor Unit

The basic functional unit consisting of an anterior horn cell, its axon, and all muscle fibers it innervates. In EMG, refers to the electrical signal generated by voluntary contraction of this unit.

Recruitment

The activation of additional motor units as the force of muscle contraction increases. Normal recruitment follows the size principle: small motor units recruited before large ones.

Interference Pattern

The EMG pattern during maximal voluntary contraction when individual motor units cannot be distinguished. Reduced interference pattern suggests loss of motor units (neurogenic process).

Polyphasic Potentials

Motor unit potentials with 5 or more phases (baseline crossings). Up to 15% polyphasic potentials can be normal. Increased polyphasia suggests reinnervation or muscle disease.

MUAP (Motor Unit Action Potential)

The electrical signal recorded from a motor unit during voluntary contraction. Analyzed for amplitude, duration, and morphology to assess for neurogenic or myopathic changes.

Neurogenic Changes

EMG findings suggesting nerve or anterior horn cell pathology: increased MUAP amplitude and duration, reduced recruitment, abnormal spontaneous activity, and increased polyphasia during reinnervation.

Myopathic Changes

EMG findings suggesting primary muscle disease: decreased MUAP amplitude and duration, early/excessive recruitment, and sometimes abnormal spontaneous activity in inflammatory myopathies.

Conduction Block

Failure of action potential propagation along a nerve segment, resulting in significant amplitude drop (>50%) without corresponding prolongation of distal latency. Suggests demyelinating neuropathy.

Temporal Dispersion

Prolongation and widening of the compound action potential due to variable conduction velocities of individual axons. Often accompanies conduction block in demyelinating neuropathies.

F-waves

Late responses resulting from antidromic activation of anterior horn cells. Used to assess proximal nerve conduction and nerve root function. Normal F-wave latency rules out proximal conduction abnormalities.

H-reflex

Electrically elicited stretch reflex, most commonly tested in the calf muscles via tibial nerve stimulation. Useful for assessing S1 nerve root function and early polyneuropathy detection.

Pattern Recognition for Residents

Axonal vs. Demyelinating Patterns:

Axonal: Reduced amplitudes, normal or mildly slow velocities, normal distal latencies
Demyelinating: Prolonged distal latencies, slow velocities, conduction blocks, temporal dispersion

Nerve Injury Classification

Clinical Correlation: Understanding nerve injury classification helps predict recovery and guide treatment decisions. EMG findings evolve over time based on injury severity.

Neurapraxia (Sunderland Grade 1)

Pathology: Temporary loss of nerve function due to focal demyelination

EMG Findings:
• Conduction block across lesion
• Normal distal conduction
• No denervation changes
• Recovery: Days to weeks

Axonotmesis (Sunderland Grades 2-4)

Pathology: Axon disruption with intact endoneurium (Grade 2) to perineurium/epineurium damage (Grades 3-4)

EMG Findings:
• Loss of voluntary motor units
• Fibrillations and positive sharp waves
• Reduced/absent compound action potentials
• Recovery: Months, may be incomplete

Neurotmesis (Sunderland Grade 5)

Pathology: Complete nerve transection with disruption of all neural structures

EMG Findings:
• Complete loss of nerve function
• Absent compound action potentials
• Extensive denervation changes
• Recovery: Requires surgical repair

Seddon Classification (Simplified)

Neurapraxia: Temporary loss, full recovery expected
Axonotmesis: Axon damage, variable recovery
Neurotmesis: Complete severance, requires surgery

EMG Timing After Nerve Injury

0-7 days: Motor units still responsive distal to lesion
7-10 days: Distal motor responses begin to decline
2-3 weeks: Fibrillations and positive sharp waves appear
3-6 months: Reinnervation changes may appear (polyphasic MUAPs)
6-12 months: Chronic changes stabilize

Quick Reference Guide

Normal Values Summary

Sensory NCS:
• Amplitude: >10-15 μV
• Velocity: >50 m/s
• Peak Latency: <3.5 ms

Motor NCS:
• Amplitude: >4-6 mV (varies by nerve)
• Velocity: >50 m/s (arm), >44 m/s (leg)
• Distal Latency: <4.4 ms (varies by nerve)

Axonal vs Demyelinating Criteria

Axonal Loss Pattern:
• Reduced amplitudes (primary finding)
• Normal or mildly slow CV (never <75% LLN)
• Normal or mildly prolonged DL (never >130% ULN)
• No change in waveform morphology

Demyelinating Pattern:
• Markedly slow CV (<75% LLN or <35 m/s arm/<30 m/s leg)
• Markedly prolonged DL (>130% ULN)
• May have conduction block/temporal dispersion
• Amplitudes may be reduced (especially sensory)

Conduction Block Criteria

Motor Conduction Block:
• >50% drop in area between distal/proximal sites
• >20% drop suggests possible block
• Often associated with temporal dispersion
• Duration increase >15% = abnormal dispersion

Clinical Significance:
• Indicates acquired demyelination
• Good prognosis (remyelination possible)
• Differentiates from axonal loss

Normal Sensory NCS Patterns

Root Lesions:
• Normal SNAPs (DRG intact)
• Abnormal needle EMG in myotome
• Motor NCS may be abnormal

Peripheral Nerve Lesions:
• Abnormal SNAPs in nerve distribution
• Abnormal motor NCS in same nerve
• Needle EMG abnormal in nerve distribution

Common Technical Pitfalls

Temperature Effects:
• Cold limbs (keep >32°C)
• 2°C cooling = 5% velocity decrease

Stimulation Errors:
• Submaximal stimulation
• Co-stimulation of adjacent nerves
• Poor electrode contact

Measurement Errors:
• Inaccurate distance measurement
• Wrong latency markers
• Baseline drift artifacts

When to Order EMG/NCS

Appropriate Indications:
• Localize nerve lesions
• Differentiate neurogenic vs. myopathic
• Assess severity and prognosis
• Monitor disease progression
• Evaluate weakness of unknown cause

Not Indicated For:
• Chronic back pain without radiculopathy
• Fibromyalgia or chronic pain syndromes
• Central nervous system disorders
• Pure sensory symptoms with normal exam

Quick Clinical Decision Tree

Fast decision making for EMG/NCS clinical scenarios:

Weakness Pattern Analysis:
• Distal symmetrical → Polyneuropathy (NCS first)
• Proximal symmetrical → Myopathy (EMG first)
• Asymmetrical → Mononeuropathy/radiculopathy (NCS + EMG)
• Upper motor neuron signs → EMG/NCS NOT indicated

Sensory Loss Patterns:
• Glove/stocking → Polyneuropathy
• Dermatomal → Radiculopathy
• Specific nerve distribution → Mononeuropathy

Quick Decision Rules:
• Normal SNAPs + clinical sensory loss = Proximal to DRG
• Amplitude ↓ = Axonal injury
• Velocity/Latency ↓ = Demyelination
• Always check temperature (>32°C required)

📹 NCS/EMG Video Library

Curated collection of educational videos covering nerve conduction study techniques, electrode placement, and EMG interpretation methods for comprehensive learning.

📖 Cardinal Rules of NCS (Preston & Shapiro)

Essential principles that every resident must master for successful nerve conduction studies. These fundamental rules form the foundation of accurate EMG/NCS practice and interpretation.

🎯 Cardinal Rules of NCS

Essential principles that every resident must remember

Clinical Correlation First

NCS are an extension of the clinical examination - Always correlate findings with clinical symptoms

Technical Factors Rule

When in doubt, think technical factors - Most "abnormalities" are technical errors

Reexamine When Needed

When in doubt, reexamine the patient - If findings don't match exam, recheck both

Supramaximal Stimulation

Use supramaximal stimulation - Increase current 20% beyond plateau

Optimize Stimulator Position

Find lowest threshold, then increase to supramaximal

Don't Overcall Abnormalities

Minor findings without clinical correlation may be irrelevant

🎓 SENIOR RESIDENT LEVEL

🧬 Advanced Muscle Laboratory

Preston & Shapiro Complete Muscle Database

Muscles

∞

Questions

📈

Adaptive

Region

🧪 Interactive Quiz

🎯 Select Quiz Types

Choose which anatomical concepts to test (independent of display mode)

⚡

Peripheral Nerves

Test nerve supply knowledge

Active

🌿

Nerve Roots

Test root level knowledge

Active

🔗

Brachial Plexus Cords

Test cord level knowledge

Active

🌳

Brachial Plexus Trunks

Test trunk level knowledge

Active

💪

Muscle Actions

Test functional knowledge

Active

Test your knowledge with adaptive questions

Quiz Mode:

📋 Anatomy Display Controls

Choose what anatomical information to show on the muscle cards below

🎓 SENIOR RESIDENT LEVEL

🧠 EMG Localization Challenge

Sharpen your advanced muscle localization skills with this expert-level quiz system that presents dynamic, contextual questions about EMG findings and complex muscle anatomy patterns. Perfect for senior residents preparing for board examinations and fellowship training.

⚠️

Expert-Level Clinical Tool

This advanced challenge is designed for senior residents and fellows with substantial EMG experience. Prerequisites include:

✓ Extensive EMG needle examination experience
✓ Advanced understanding of denervation patterns
✓ Clinical correlation and localization expertise
✓ Familiarity with complex anatomical variations

This tool simulates real clinical scenarios with complex denervation patterns requiring expert-level interpretation skills.

📋 Challenge Configuration

Configure your advanced EMG localization challenge parameters

🎯 Select Question Types

Choose which types of localizations you want to practice

🌿

Nerve Root Lesions

C5-T1, L2-S1 radiculopathies

Examples: C6 radiculopathy, L5 radiculopathy

Active

🌳

Plexus Trunk Lesions

Upper, middle, lower trunk injuries

Examples: Erb's palsy, Klumpke's palsy

Active

🔗

Plexus Cord Lesions

Lateral, posterior, medial cord injuries

Examples: Lateral cord palsy, posterior cord injury

Active

⚡

Peripheral Nerve Lesions

Entrapment neuropathies, focal injuries

Examples: Carpal tunnel, peroneal palsy

Active

At least one question type must be selected

💼 Clinical Scenario

Loading clinical scenario...

⚡ EMG Needle Examination Results

❌ Abnormal Muscles (Denervation)

✅ Normal Muscles

🧠 Analysis Question

Where is the most likely location of the lesion?

🧬 Nerve Physiology

Comprehensive understanding of cellular and molecular mechanisms underlying nerve function, conduction, synaptic transmission, and pathophysiology. Essential physiological concepts for advanced EMG/NCS interpretation.

⚡ Action Potential Cascade

The electrical foundation of neural communication - Understanding the precise molecular events that generate and propagate electrical signals in nerve fibers

The action potential represents the fundamental unit of information transfer in the nervous system. This all-or-nothing electrical event involves precisely coordinated molecular changes across the nerve membrane that create a propagating wave of depolarization. Understanding these mechanisms is critical for interpreting EMG/NCS abnormalities and localizing neurological lesions.

🔋

Resting Potential

-70mV to -90mV

Na+/K+-ATPase pump (3:2 ratio)
K+ leak channels dominant
Impermeant anions trapped inside
Electrochemical equilibrium

🏥 Clinical: Resting potential changes in neuropathies affect excitability

🚀

Depolarization

Threshold: -55mV

Voltage-gated Na+ channels open
Positive feedback loop
Fast Na+ conductance (0.1-0.2ms)
Peak: +30 to +40mV

🏥 Clinical: Na+ channel dysfunction = muscle weakness, myotonia

📉

Repolarization

K+ efflux dominant

Na+ channels inactivate
Delayed K+ channels open
Membrane returns to rest
Brief hyperpolarization

🏥 Clinical: K+ channel disorders = periodic paralysis

🏃‍♂️ Conduction Velocity Secrets

What makes nerves fast or slow

🛡️

Myelination

Saltatory Conduction

Nodes of Ranvier (1-2μm gaps)
High Na+ channel density at nodes
Internodal length: 150-1500μm
50x faster than unmyelinated

Formula: CV = 6 × diameter (μm) m/s

📏

Axon Diameter

Size Matters

Large axons = faster conduction
Motor > Sensory > Autonomic
Temperature coefficient: 2.4%/°C
Aging: 0.4 m/s decrease per decade

Fiber Types:

Aα (70-120 m/s) > Aβ (30-70 m/s) > C (0.5-2 m/s)

⚠️

Pathological Changes

Disease Effects

Demyelination: ↓ velocity, ↑ latency
Axonal loss: ↓ amplitude
Conduction block: amplitude drop
Temporal dispersion: duration ↑

🏥 Clinical: Pattern determines neuropathy type

🔗 Synaptic Transmission

Neuromuscular junction mechanics

📡

Presynaptic Events

Ca²⁺-Mediated Release

Voltage-gated Ca²⁺ channels
SNARE protein complex
Vesicle fusion & exocytosis
ACh quantum release

🏥 Clinical: Lambert-Eaton affects Ca²⁺ channels

⚡

Synaptic Cleft

20-50nm Gap

ACh diffusion time: 0.2ms
Acetylcholinesterase breakdown
Safety factor: 3-4x
Miniature EPPs: 0.4mV

🏥 Clinical: Organophosphates block AChE

🎯

Postsynaptic Response

Nicotinic ACh Receptors

Pentameric structure (2α,β,δ,ε)
Na⁺/K⁺ non-selective channel
EPP → Muscle action potential
All-or-nothing response

🏥 Clinical: Myasthenia gravis attacks AChR

🧪 Membrane Chemistry

Ion channels and molecular machinery

🚪

Ion Channel Types

Selective Permeability

Voltage-gated: Na⁺, K⁺, Ca²⁺
Ligand-gated: ACh, GABA, Gly
Mechanosensitive channels
Leak channels: K⁺ dominant

Properties: Selectivity, gating, inactivation

⚙️

Active Transport

Energy-Dependent

Na⁺/K⁺-ATPase: Primary pump
Ca²⁺-ATPase: Muscle relaxation
H⁺-ATPase: pH regulation
Secondary transport systems

🏥 Clinical: Digitalis blocks Na⁺/K⁺ pump

🫧

Membrane Structure

Phospholipid Bilayer

Hydrophobic core barrier
Cholesterol: fluidity control
Membrane proteins: 50% mass
Capacitance: 1 μF/cm²

🏥 Clinical: Membrane instability in channelopathies

💪 Muscle Fiber Physiology

Excitation-contraction coupling and fiber types

⚡

E-C Coupling

Signal Transduction

T-tubule system
Sarcoplasmic reticulum
Ca²⁺ release & uptake
Troponin/tropomyosin

🏥 Clinical: Malignant hyperthermia = RYR1 mutations

🏃

Fiber Types

Motor Unit Properties

Type I: Slow, oxidative
Type IIa: Fast, oxidative
Type IIx: Fast, glycolytic
Recruitment order by size

🏥 Clinical: Fiber type grouping in reinnervation

🔥

Energy Systems

ATP Generation

Creatine phosphate: Immediate
Glycolysis: Short-term
Oxidative: Long-term
Metabolic demand varies

🏥 Clinical: Metabolic myopathies affect energy

🧵 Nerve Fiber Classification

The complete nerve highway system - Understanding the different "lanes" of neural traffic (Preston & Shapiro)

Think of nerves as superhighways with multiple lanes carrying different types of information at different speeds. Just like express lanes handle fast traffic while local lanes carry slower vehicles, nerve fibers are classified by size and speed. Larger fibers = faster conduction, smaller fibers = slower speeds. This classification system is crucial for understanding what EMG/NCS can and cannot detect!

💪

Motor Highway

The express lane for movement commands

Aα Motor Fibers

6-12 μm diameter

35-75 m/s

EXPRESS LANE

The VIP lane of the nervous system! These thick, myelinated superhighways carry movement commands from your brain to muscles.

What they do:

🎯 Voluntary muscle contraction
⚡ Alpha motor neuron signals
💪 All the movements you control
🏃‍♂️ Fast, precise motor commands

✅ EASILY RECORDED

Routine motor NCS: These are exactly what we measure in standard EMG/NCS studies. CMAP amplitudes reflect how many of these fibers are working!

🏥 Clinical Pearl: When motor NCS are abnormal, these Aα fibers are damaged. The bigger the amplitude drop, the more fibers are gone!

👋

Sensory Highway

Multiple lanes for different sensations

Aβ Sensory Fibers

6-12 μm diameter

35-75 m/s

EXPRESS LANE

The touch and vibration superhighway! Same size and speed as motor fibers, but carrying sensory information up to your brain.

What they carry:

👋 Light touch sensation
📳 Vibration (tuning fork tests)
🤏 Fine discriminative touch
📍 Joint position sense

✅ EASILY RECORDED

Routine sensory NCS: These create the SNAPs we measure! When you stimulate a finger and record from the wrist, you're testing Aβ fibers.

🏥 Clinical Pearl: Diabetic neuropathy often hits these first. Patient loses vibration sensation, but SNAPs may still be recordable early on.

Aδ Pain Fibers

1-5 μm diameter

5-30 m/s

LOCAL LANE

The "fast pain" messengers! Smaller and slower than Aβ, but still myelinated. Think sharp, immediate pain like a pinprick.

What they carry:

⚡ Sharp, fast pain
🧊 Cold temperature
📍 Initial pain sensation
⚠️ "Ouch!" reflexes

❌ NOT RECORDED

Too small for routine NCS: These fibers are too thin and their signals too dispersed to create measurable potentials in standard studies.

🏥 Clinical Pearl: Small fiber neuropathy affects these! Patient has burning pain but normal EMG/NCS. Need special tests like skin biopsy.

C Pain Fibers

0.2-1.5 μm diameter

1-2 m/s

SLOW LANE

The "slow burn" highway! Tiny, unmyelinated fibers that carry the deep, aching, burning sensations. These are the smallest and slowest in the nervous system.

What they carry:

🔥 Burning, aching pain
🌡️ Heat sensation
😣 Chronic pain signals
💔 Deep, throbbing discomfort

❌ NOT RECORDED

Way too small for NCS: No myelin, incredibly slow, and signals are too dispersed. Standard EMG/NCS completely misses these fibers.

🏥 Clinical Pearl: Fibromyalgia, early diabetes, chemotherapy neuropathy often affect C-fibers. Normal EMG/NCS doesn't rule out neuropathy!

🏆

VIP Express Lane

The muscle feedback specialists

Ia Muscle Afferents

12-21 μm diameter

80-120 m/s

VIP EXPRESS

The fastest fibers in your body! These massive, heavily myelinated superhighways are larger and faster than anything else in the nervous system. They're the muscle stretch sensors.

What they do:

🎯 Muscle stretch detection
⚡ Knee-jerk reflex pathways
🤸‍♂️ Proprioception (body position)
⚖️ Balance and coordination

⚠️ MIXED NERVE ONLY

Special studies required: Only recorded in mixed nerve studies or H-reflexes. Too fast and specialized for routine sensory NCS.

🏥 Clinical Pearl: First affected in demyelinating diseases like GBS! Early loss of reflexes before weakness. Check H-reflexes early!

🎯 Key Clinical Takeaways

What this means for your EMG/NCS interpretation

⚠️

NCS Limitations

Standard EMG/NCS only sees the "express lanes"! We miss small fiber neuropathies, early autonomic problems, and pure pain/temperature issues.

🛡️

Demyelination Clues

Big fibers affected first! Ia fibers (reflexes) → Aα/Aβ (strength/touch) → small fibers last. Explains why reflexes disappear before weakness.

✅

Normal Studies Don't Rule Out Neuropathy

50% of nerve fibers could be gone and NCS still normal! Small fibers aren't measured, so burning feet with normal studies is totally possible.

🎯 Interactive Learning

Test your physiological knowledge

❓

Physiology Quiz

Test membrane potential, action potential, and synaptic transmission concepts

📊

Virtual Oscilloscope

Visualize action potentials, EPPs, and compound muscle action potentials

🧮

Physiology Calculator

Calculate membrane potentials, conduction velocities, and safety factors

🔬 Pathophysiology Patterns

Disease mechanisms and EMG/NCS correlations - The two fundamental patterns of nerve injury

All nerve pathology fundamentally falls into two main patterns: axonal injury (the nerve fibers themselves are damaged) and demyelinating injury (the insulation is damaged but fibers remain intact). Understanding these patterns is crucial for EMG/NCS interpretation and determining prognosis.

💥

Axonal Injury

Mechanism:

Axon structural damage
Wallerian degeneration
Reduced axon number

EMG/NCS Changes:

🔽 Amplitude (CMAP/SNAP)
✅ Normal velocity
⚡ Fibrillations/PSWs
🔄 Chronic: large MUPs

Examples: Diabetes, chemotherapy, alcohol

🏥 Clinical: Poor prognosis, recovery depends on regeneration

🛡️

Demyelinating

Mechanism:

Myelin sheath damage
Saltatory conduction loss
Conduction block

EMG/NCS Changes:

🐌 Slow velocity
⏰ Prolonged latency
🚧 Conduction block
📏 Temporal dispersion

Examples: CIDP, GBS, CMT1

🏥 Clinical: Better prognosis, remyelination possible

⏰ Wallerian Degeneration Timeline

Critical timing for interpreting acute nerve injuries - Understanding the precise temporal sequence of axonal degeneration

Wallerian degeneration represents the predictable breakdown of axons distal to a site of injury. This process follows a precise timeline that is crucial for EMG/NCS interpretation in acute nerve injuries. Understanding these phases helps clinicians time their studies appropriately and interpret seemingly "normal" results in the acute setting.

Day 0-3

Immediate Phase

Normal distal NCS despite proximal nerve injury

Mechanism: Distal axon still viable, normal excitability maintained

Day 3-5

Motor Decline

Motor responses begin to decline

Mechanism: Large motor axons degenerate first, CMAP amplitudes drop

Day 6-10

Sensory Decline

Sensory responses begin to decline

Mechanism: Sensory axons follow motor degeneration, SNAP amplitudes drop

Day 7-10

Complete Loss

Distal nerve becomes inexcitable

Mechanism: Axonal membrane breakdown, complete conduction failure

Week 2-3

EMG Changes

Fibrillations appear on needle EMG

Mechanism: Denervated muscle fibers become hyperexcitable

Month 3-6

Recovery Phase

Reinnervation potentials appear if recovery occurs

Mechanism: Axonal sprouting and muscle reinnervation

⚠️

Critical Clinical Point

Normal NCS in the first week don't exclude severe nerve injury! Always consider the timeline when interpreting acute studies.

📡 Volume Conduction Principles

Understanding how electrical signals travel from nerve/muscle to recording electrodes

Volume conduction describes how bioelectric potentials spread through conductive tissues to reach recording electrodes. This fundamental concept explains the shape, size, and timing of recorded potentials and is essential for understanding EMG/NCS waveform morphology.

📶

Near-field Potentials

Most NCS record near-field potentials

CMAPs and SNAPs are near-field
Electrode close to source
High amplitude recordings
Sharp, well-defined waveforms

🏥 Clinical: Proper electrode placement critical for amplitude

〰️

Waveform Types

Shape depends on source location

Triphasic: Advancing action potential
Biphasic: Starting under electrode
Positive→negative→positive phases
Duration reflects propagation time

🏥 Clinical: Waveform morphology indicates proximity

📏

Distance Effects

Amplitude decreases with distance

Inverse square law relationship
Far-field: stimulus artifact
Appears instantly at all sites
Low amplitude, wide distribution

🏥 Clinical: Explains why proximal responses smaller

⏰ Temporal Dispersion & Phase Cancellation

Why proximal sensory responses are smaller and longer in duration

As nerve impulses travel over longer distances, faster and slower conducting fibers arrive at recording sites at different times. This temporal dispersion creates phase cancellation effects that reduce amplitude and increase duration - a normal phenomenon that becomes pathologically enhanced in demyelinating conditions.

⚡

Temporal Dispersion

Fast fibers arrive before slow fibers

Normal fiber velocity variation
Increases with distance
Creates "smeared" waveforms
Duration increases proximally

Effect: Duration ∝ Distance ÷ Velocity

❌

Phase Cancellation

Overlapping phases reduce amplitude

Positive phase of fast fibers
Overlaps negative phase of slow fibers
Net amplitude reduction
More prominent proximally

🏥 Clinical: Normal proximal SNAP reduction

⚠️

Pathological Enhancement

Disease worsens these effects

Demyelination increases dispersion
Greater velocity variation
Excessive phase cancellation
Motor studies less affected

🏥 Clinical: Hallmark of demyelinating neuropathy

🌿 Radiculopathy Pathophysiology

Understanding nerve root lesions and their unique EMG/NCS patterns

Radiculopathies present unique challenges for EMG/NCS interpretation because the lesion occurs proximal to the dorsal root ganglion. This anatomical relationship creates characteristic patterns that distinguish root lesions from more peripheral nerve injuries.

🏗️

Anatomical Considerations

Proximal to DRG location

Lesion proximal to dorsal root ganglion
Sensory cell bodies intact
Distal sensory axons preserved
Normal sensory conduction studies

🏥 Clinical: Normal SNAPs with sensory loss

💪

Motor Involvement

Selective muscle denervation

Only root-innervated muscles affected
Myotomal distribution pattern
Multiple nerve involvement
Paraspinal muscle changes

🏥 Clinical: Multiple nerve territory involvement

⏱️

Temporal Patterns

Specific timing sequence

Paraspinals abnormal first (7-10 days)
Proximal muscles next (2-3 weeks)
Distal muscles last (3-4 weeks)
H-reflex changes early

🏥 Clinical: Timing guides needle EMG planning

🚧 Conduction Block Mechanisms

Understanding focal demyelination and its effects on nerve conduction

Conduction block represents focal failure of impulse propagation through an otherwise intact axon. This phenomenon occurs when demyelination or compression creates sufficient impedance to prevent action potential propagation, resulting in amplitude drops without velocity changes.

🔬

Mechanism

Focal demyelination effects

Local myelin loss or thinning
Increased membrane capacitance
Current leak at demyelinated node
Insufficient current for propagation

🏥 Clinical: Reversible with remyelination

🎯

NCS Detection

Amplitude drop criteria

>50% amplitude drop across segment
Normal distal latency
Normal or mildly slow velocity
May see temporal dispersion

🏥 Clinical: Indicates demyelinating pathology

🔄

Recovery Patterns

Remyelination timeline

Block may resolve in weeks-months
Remyelination restores conduction
Thinner myelin = slower velocity
Complete recovery possible

🏥 Clinical: Better prognosis than axonal loss

Interactive EMG/NCS Case Studies

Ready to test your EMG/NCS knowledge?

⚡ Choose Your Challenge Level

🎯 Select Your Cases

📋 Patient Presentation

🔍 Physical Examination Findings

🧠 Build Your Differential Diagnosis

⚖️ Clinical Decision: EMG/NCS Indication

⚡ Nerve Conduction Study Results

🔬 EMG Results (when required for diagnosis)

🎯 Final Diagnosis

Key Principles for Differential Building

Nerve Conduction Studies

⚡ Key Technical Points - Cardinal Rules of NCS

🌡️ Temperature Control

⚡ Supramaximal Stimulation

🎯 Electrode Placement

📏 Distance Measurement

🔇 Artifact Minimization

🎛️ Stimulator Optimization

Median Sensory

Ulnar Sensory

Dorsal Ulnar Cutaneous (DUC)

Radial Sensory

Median Motor

Ulnar Motor

Fibular (Peroneal) Motor

Tibial Motor

Sural Sensory

Median Sensory - Ring Finger (Mixed)

Median Sensory - Thumb

Median Motor - 2nd Lumbrical

Ulnar Sensory - Little Finger

Ulnar Motor - First Dorsal Interosseous

Radial Sensory - Superficial Branch

Radial Motor - Extensor Indicis

Lateral Antebrachial Cutaneous

Medial Antebrachial Cutaneous

Median-Ulnar Comparison Studies

Axillary Motor

Suprascapular Motor

Long Thoracic Motor

Spinal Accessory Motor

Cardinal Rules of NCS (Preston & Shapiro)

Key Technical Points

Volume Conduction Principles

Temporal Dispersion & Phase Cancellation

Orthodromic vs Antidromic Studies

Basic Nerve Physiology for NCS

Nerve Fiber Classification (Preston & Shapiro)

Mixed Nerve Studies

Wallerian Degeneration Timeline

EMG Machine Components & Needles

Amplifier

Filters

Stimulator

Display Monitor

Audio System

Ground Electrode

EMG Needle Types

Monopolar Needle

Concentric Needle

Single Fiber Needle

Essential EMG Terminology

Pattern Recognition for Residents

Nerve Injury Classification

Neurapraxia (Sunderland Grade 1)

Axonotmesis (Sunderland Grades 2-4)

Neurotmesis (Sunderland Grade 5)

Seddon Classification (Simplified)

EMG Timing After Nerve Injury

Quick Reference Guide

Normal Values Summary

Axonal vs Demyelinating Criteria

Conduction Block Criteria

Normal Sensory NCS Patterns

Common Technical Pitfalls

When to Order EMG/NCS

Quick Clinical Decision Tree