Peripheral Nerve Conduction Patterns
Demyelinating peripheral neuropathy is identified on nerve conduction studies by slowed conduction and segmental loss of myelin function, typically expressed as slowed conduction velocity, prolonged distal latency, temporal dispersion, and conduction block. [1–3] Axonal peripheral neuropathy is identified by reduced nerve action potential amplitudes (CMAP and SNAP) that reflect axonal loss, with comparatively less prominent slowing of conduction parameters. [2,4]
Clinical Clues With Electrodiagnostic Correlates
Demyelination is often associated with weakness that can show a conduction-block pattern and sensory involvement that may be variable depending on the specific syndrome. [2,3] Axonal loss is often associated with progressive weakness and sensory loss patterns that correlate with reduced CMAP/SNAP amplitudes on electrodiagnostic testing. [2,4]
Nerve Conduction Study Criteria for Demyelination
Demyelination is supported by slowed conduction velocity (slower than 75% of the lower limit of normal). [2] Demyelination is supported by marked distal latency prolongation (longer than 130% of the upper limit of normal). [2] Demyelination is supported by temporal dispersion, which is reflected by increased CMAP duration after proximal stimulation compared with distal stimulation. [1,3] Demyelination is supported by conduction block, which is reflected by a proximal drop in CMAP amplitude (or area) relative to distal stimulation, with criteria commonly used in immune-mediated demyelinating neuropathies. [1,3]
Conduction Block and Temporal Dispersion Measurements
Motor conduction block is commonly defined in immune-mediated demyelinating neuropathies as a reduction of proximal-to-distal CMAP amplitude by at least 30%, with additional safeguards regarding distal amplitude. [3] F-wave latency prolongation supports demyelination and is commonly defined in immune-mediated demyelinating neuropathy criteria as a prolongation of at least 20% above the upper limit of normal in multiple nerves. [3] Temporal dispersion supports demyelination as a relative prolongation of CMAP duration in proximal segments compared with distal segments. [1,3]
Findings Characteristic of Axonal Loss
Axonal loss is identified by reduced CMAP and/or SNAP amplitudes on nerve conduction studies, reflecting decreased numbers of functioning axons. [2,4] Axonal loss may produce conduction slowing secondary to preferential loss of fast-conducting fibers, which can mimic demyelination without true segmental demyelinating physiology. [3] On needle EMG, axonal neuropathy typically shows denervation and reinnervation features that reflect ongoing axonal injury and regeneration. [4]
Mononeuropathy Versus Polyneuropathy Patterns
Focal demyelination across a lesion site supports a demyelinating entrapment or focal demyelinating process when segmental abnormalities localize to a specific anatomical segment. [2] Length-dependent axonal polyneuropathy supports a distal symmetric pattern that correlates with progressively reduced amplitudes distally. [4]
Practical Electrodiagnostic Interpretation Algorithm
Segmental demyelination is prioritized when conduction slowing and/or conduction block and/or temporal dispersion are present in nerves tested outside common entrapment sites. [3,5] Predominant axonal neuropathy is prioritized when CMAP/SNAP amplitudes are reduced with comparatively preserved conduction velocities and without clear evidence of conduction block. [2,4] Mixed neuropathy is prioritized when both axonal loss (reduced amplitudes) and demyelinating features (slowed conduction and/or conduction block/temporal dispersion) coexist in the same study. [2,4]
Important Pitfalls and Limitations
Conduction block and temporal dispersion can be difficult to interpret when axonal loss is severe, because absent or markedly reduced motor potentials can reduce test sensitivity for demyelinating criteria. [3] Some patients can have immune-mediated demyelinating neuropathy with partial or insufficient electrodiagnostic fulfillment of demyelination criteria, particularly in sensory-predominant variants with absent SNAPs. [3] Technical issues and entrapment neuropathies can confound interpretation, so localization and comparison across segments and nerves are required. [2,3]
Common Helpful Next Steps
Electrodiagnostic studies should include both sensory and motor studies when feasible to distinguish demyelinating versus axonal patterns and to characterize distribution. [4] When immune-mediated demyelinating neuropathy is a concern, applying formal demyelination criteria (including conduction block, temporal dispersion, distal latency, and F-wave latency measures) across multiple nerves supports diagnostic classification. [3]
Targets for Confirmation of True Demyelination
True demyelination is confirmed when objective demyelinating physiology is demonstrated, typically using criteria based on slowed conduction velocity, prolonged distal latency, and/or conduction block with temporal dispersion in multiple nerves. [2,3] Axonal neuropathy is confirmed when the dominant abnormality is reduced CMAP/SNAP amplitudes without convincing segmental conduction failure. [2,4]