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Electrodiagnostic Medicine: Principles of NCS and EMG

Overview

Electrodiagnostic (EDx) studies are an extension of the neurological examination, comprising nerve conduction studies (NCS) and needle electromyography (EMG). They are essential for localizing, characterizing, and prognosticating neuromuscular disorders and should always be interpreted in clinical context rather than as a substitute for clinical assessment. Timing is a critical consideration: Wallerian degeneration takes 7-10 days to complete, and denervation potentials on EMG do not appear until 2-3 weeks after nerve injury.

Nerve Conduction Studies (NCS)

Motor NCS

Motor NCS involve supramaximal stimulation of a motor nerve while recording from a muscle in its territory. The CMAP amplitude reflects the number of functioning motor axons and is reduced in axonal neuropathy, motor neuron disease, NMJ disorders, and myopathy. The distal motor latency (DML) is the time from distal stimulation to CMAP onset and is prolonged in distal demyelination or entrapment. Conduction velocity (CV) is calculated by dividing the distance between proximal and distal stimulation sites by the latency difference, and is reduced in demyelinating neuropathies. CMAP duration is prolonged with temporal dispersion, which indicates acquired demyelination.

Sensory NCS

Sensory NCS involve stimulating a sensory or mixed nerve and recording the sensory nerve action potential (SNAP). SNAP amplitude reflects the number of sensory axons and is reduced in sensory neuropathies and axonal lesions distal to the dorsal root ganglion (DRG). Sensory conduction velocity is slowed in demyelinating neuropathies. A key principle is that SNAP is preserved in preganglionic lesions (radiculopathy, plexopathy proximal to DRG) because the cell body in the DRG and the distal axon remain intact.

F-Waves

F-waves are late responses generated by antidromic activation of motor neurons in the spinal cord. They have variable latency and morphology because different motor neurons fire with each stimulus. F-waves are prolonged or absent in demyelinating neuropathies, especially those affecting proximal nerve segments as in GBS. They are assessed by the minimum F-wave latency.

H-Reflex

The H-reflex is the electrical equivalent of the monosynaptic stretch reflex (ankle jerk), most reliably obtained from the soleus muscle with tibial nerve stimulation. It is prolonged or absent in S1 radiculopathy, polyneuropathy, or proximal demyelination, and is one of the earliest abnormalities detectable in GBS.

<image>Diagram showing the setup and waveform components of motor and sensory nerve conduction studies including CMAP amplitude, distal latency, conduction velocity measurement, and F-wave</image>

Distinguishing Axonal from Demyelinating Neuropathy on NCS

ParameterAxonal PatternDemyelinating Pattern
CMAP/SNAP amplitudeReducedPreserved early; reduced late
Conduction velocityNormal or mildly reducedSlowed (<70% LLN)
Distal motor latencyNormal or mildly prolongedProlonged (>130-150% ULN)
F-wave latencyNormalProlonged or absent
Conduction blockAbsentPresent (>50% amplitude drop)
Temporal dispersionAbsentPresent (>30% duration increase)

Axonal Pattern

The axonal pattern is characterized by reduced CMAP and/or SNAP amplitudes with normal or near-normal conduction velocities (which may be mildly reduced due to loss of the fastest-conducting fibers), normal distal latencies (or mildly prolonged), normal F-wave latencies, and no conduction block or temporal dispersion.

Demyelinating Pattern

The demyelinating pattern shows slowed conduction velocities (below 70% of the lower limit of normal), prolonged distal motor latencies (above 130-150% of the upper limit of normal), prolonged F-wave latencies, temporal dispersion (increased CMAP duration greater than 30%), and conduction block (greater than 50% CMAP amplitude drop between proximal and distal stimulation). SNAP and CMAP amplitudes may be preserved early in demyelinating disease.

Conduction Block

Definite conduction block is defined as greater than 50% reduction in proximal CMAP amplitude compared to distal CMAP amplitude with less than 15% change in duration. It indicates acquired demyelination at the site of the block, as seen in CIDP, GBS, and MMN. Conduction block is not seen in hereditary demyelinating neuropathies (CMT1 produces uniform slowing) and must be interpreted carefully at common entrapment sites.

Uniform vs. Non-Uniform Demyelination

Uniform demyelination, in which all nerves show a similar degree of slowing, suggests a hereditary process such as CMT1A or CMT1B. Non-uniform demyelination, with variable involvement across nerves accompanied by conduction block and temporal dispersion, suggests an acquired process such as CIDP, GBS, or anti-MAG neuropathy.

Needle Electromyography (EMG)

Components of the EMG Examination

Insertional Activity

Normal insertional activity consists of a brief burst of electrical activity upon needle insertion. Increased insertional activity (fibrillations, positive sharp waves, myotonic discharges) indicates denervation or active myopathy. Decreased insertional activity indicates end-stage muscle with fibrosis and fatty replacement.

Spontaneous Activity (at Rest)

Fibrillation potentials are spontaneous discharges of a single muscle fiber indicating denervation, active myopathy, or NMJ disruption. Positive sharp waves (PSWs) have the same clinical significance as fibrillations but different morphology. Fasciculation potentials are spontaneous discharges of an entire motor unit, seen in ALS, radiculopathy, and benign fasciculation syndrome. Myotonic discharges produce a characteristic waxing and waning frequency and amplitude (the "dive bomber" sound) and are seen in myotonic dystrophy, myotonia congenita, and paramyotonia. Complex repetitive discharges (CRDs) are regular, repetitive complex waveforms with a machine-like sound, seen in chronic neurogenic and myopathic conditions. Myokymic discharges are grouped, repetitive motor unit firings associated with radiation injury, GBS, and MS.

Motor Unit Action Potential (MUAP) Analysis

MUAP amplitude reflects the number and size of muscle fibers in the motor unit. Duration reflects the territory of the motor unit. Phases (defined as the number of baseline crossings plus one) are normally four or fewer. The recruitment pattern describes the number and firing rate of MUAPs during voluntary contraction.

Neurogenic vs. Myopathic Patterns

Neurogenic Pattern (Denervation/Reinnervation)

In the acute stage, fibrillations and PSWs are present with normal-appearing MUAPs but reduced recruitment (fewer motor units firing at faster rates to compensate). In the chronic stage, large-amplitude, long-duration, polyphasic MUAPs develop from collateral reinnervation sprouting, with reduced recruitment. An active plus chronic pattern shows fibrillations and PSWs alongside large, polyphasic MUAPs.

Myopathic Pattern

The myopathic pattern is characterized by small-amplitude, short-duration, polyphasic MUAPs with early recruitment (many motor units fire at low force levels because each unit generates less force). Fibrillations and PSWs may or may not be present; when they are present, the myopathy is termed "irritable" (as in inflammatory myopathies), while they are typically absent in many chronic myopathies.

<image>EMG tracings comparing normal motor unit potentials with neurogenic changes (large amplitude, long duration, reduced recruitment) and myopathic changes (small amplitude, short duration, early recruitment)</image>

Common Electrodiagnostic Patterns

Carpal Tunnel Syndrome

The earliest and most sensitive finding is prolonged median sensory distal latency across the wrist. Prolonged median motor distal latency is a later finding indicating more advanced disease. Reduced median SNAP amplitude indicates axonal loss. Comparison with ulnar nerve studies is standard, with a median-ulnar latency difference greater than 0.5 ms being abnormal. EMG shows denervation in the abductor pollicis brevis (APB) in moderate-to-severe cases.

Ulnar Neuropathy at the Elbow

Findings include reduced CMAP amplitude or conduction velocity slowing across the elbow segment (greater than 10 m/s drop) and reduced ulnar SNAP amplitude. EMG demonstrates denervation in FDI, ADM, and FDP 4-5; sparing of FCU helps localize the lesion to the elbow rather than the wrist (Guyon canal).

Radiculopathy

NCS are normal because the lesion is preganglionic and SNAP is preserved. EMG shows fibrillations and PSWs in a myotomal distribution including the paraspinal muscles, with reduced recruitment of neurogenic MUAPs in the affected myotome. Paraspinal involvement distinguishes radiculopathy from plexopathy.

GBS/AIDP

The pattern includes prolonged distal latencies, slowed conduction velocities, conduction block, temporal dispersion, and absent or prolonged F-waves. The sural sparing pattern (absent median and ulnar SNAPs with a preserved sural SNAP) is relatively specific for AIDP.

ALS

ALS shows widespread active denervation (fibrillations, PSWs) in multiple body regions, large-amplitude, long-duration MUAPs with reduced recruitment reflecting chronic reinnervation, normal sensory NCS, and widespread fasciculation potentials. The split hand index demonstrates preferential involvement of APB over ADM on motor NCS.

Myasthenia Gravis

Routine NCS may be normal or show low CMAP amplitudes. Repetitive nerve stimulation at 3 Hz demonstrates a greater than 10% decremental response, most sensitively detected in proximal or facial muscles. Single-fiber EMG shows increased jitter with greater than 95% sensitivity in generalized MG.

Timing and Practical Considerations

After nerve transection, the distal nerve segment continues to conduct for 7-10 days before Wallerian degeneration occurs; SNAP and CMAP amplitudes do not decrease until after this period. Fibrillation potentials appear 2-3 weeks after denervation, meaning EMG performed too early may be falsely normal. Temperature is a critical variable: cool limbs slow conduction velocity and can mimic demyelination, so limb temperature must be maintained at or above 32 degrees C (hand) and 30 degrees C (leg). Submaximal stimulation can falsely reduce CMAP amplitude and mimic conduction block; supramaximal stimulation must always be ensured.

<image>Table summarizing key electrodiagnostic patterns in common neuromuscular diseases including CTS, radiculopathy, GBS, CIDP, ALS, MG, and myopathy</image>

Clinical Pearls

Normal sensory studies with abnormal motor studies and EMG denervation in a myotomal pattern equals radiculopathy, because the preganglionic lesion preserves SNAP. The sural sparing pattern (preserved sural SNAP with absent upper limb SNAPs) is relatively specific for GBS/AIDP and should trigger consideration of this diagnosis. Conduction block is the most specific finding for acquired demyelination; its presence in a patient with neuropathy should prompt evaluation for CIDP or MMN. Fibrillations in a myotomal distribution with paraspinal involvement confirm radiculopathy; paraspinal fibrillations do not occur in plexopathy. EDx cannot detect small fiber neuropathy because C and A-delta fibers are too small to generate measurable potentials; skin biopsy for intraepidermal nerve fiber density is the appropriate test. Timing of the study matters because an NCS/EMG performed within the first week of acute nerve injury may be normal or misleading due to incomplete Wallerian degeneration. Always warm the limb before testing, as a 1 degree C drop in temperature slows conduction velocity by approximately 1.5-2.5 m/s. Single-fiber EMG is the most sensitive test for NMJ dysfunction but is not specific to MG; any process affecting the NMJ or motor unit can cause increased jitter.

References

  • Preston DC, Shapiro BE. Electromyography and Neuromuscular Disorders: Clinical-Electrophysiologic-Ultrasound Correlations. 4th ed. Elsevier; 2020.
  • Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice. 5th ed. Oxford University Press; 2023.
  • American Association of Neuromuscular & Electrodiagnostic Medicine. Practice parameter for electrodiagnostic studies in carpal tunnel syndrome. Muscle Nerve. 2002;25(6):918-922.
  • Tankisi H, Pugdahl K, Fuglsang-Frederiksen A, et al. Pathophysiology inferred from electrodiagnostic nerve tests and classification of polyneuropathies. Clin Neurophysiol. 2005;116(7):1571-1580.
  • Daube JR, Rubin DI. Needle electromyography. Muscle Nerve. 2009;39(2):244-270.
Electrodiagnostic Medicine: Principles of NCS and EMG — figure 1
Electrodiagnostic Medicine: Principles of NCS and EMG — figure 2
Electrodiagnostic Medicine: Principles of NCS and EMG — figure 3

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