7.2 Focal Lesions, Conduction Block, Demyelination, and Temporal Dispersion

What a lesion type means on a tracing

Outline III.A.1.b items 1–5 and 7 ask you to recognize focal lesions, conduction block, diffuse processes, multifocal disorders, demyelination, and temporal dispersion on nerve conduction studies (NCS). Independent OpenExamPrep teaching treats these as waveform patterns, not as diagnoses you assign from a single millivolt. Axonal loss (item 6) and Wallerian degeneration occupy the next section. This resource is independent study material for R.NCS.T. candidates using published AAET outline topics. It is not an official AAET manual and does not publish unpublished exam cut scores.

A compound muscle action potential (CMAP) and a sensory nerve action potential (SNAP) are summed volleys. Disease can (1) slow some or all axons, (2) block some axons at a restricted site while leaving distal axon and muscle intact, (3) desynchronize arrival times, or (4) remove axons. Those four electrical behaviors are how you read lesion types. Mixing them up turns a neurapraxic Saturday-night radial palsy into an incorrect story of massive axonal loss, or turns a dispersed proximal CMAP into a fake block.

Focal lesions

A focal lesion is spatially restricted: one compression site, one stretch, one laceration, one infarct of a named nerve. Entrapments — median nerve at the wrist, ulnar nerve at the elbow, fibular (peroneal) nerve at the fibular head — are the daily examples. NCS localizes a focal lesion by showing a change across a short segment: prolonged distal latency if the lesion is distal, focal slowing of conduction velocity across the site, conduction block at the site, temporal dispersion at the site, axonal loss distal to the site after Wallerian time, or a combination.

Long-segment velocity can dilute a short lesion. A 15 mm zone of demyelination inside a 200 mm forearm segment may only shave a few meters per second off the calculated velocity. Inching (short-segment stimulation) exists to unmask that dilution. Focal does not mean always demyelinating: a focal crush can be purely axonal. Focal also does not mean always blocked: chronic compression often slows without meeting block criteria. The job is to name the site and the electrical behavior at that site, not to recite a disease name from one latency.

Conduction block

Conduction block means the impulse fails to pass a region of nerve even though the axon is still in continuity more distally. Electrically: an abnormal drop in amplitude and/or negative-peak area when you move the stimulator from a distal site to a proximal site across the suspect segment, while the distal CMAP remains relatively preserved. The muscle still has a large generator. The volley simply does not get through the bad segment.

Teaching thresholds used in demyelinating-neuropathy literature often treat a greater than about 20% amplitude drop as possible partial block, with stricter drops (commonly discussed near 50% in some motor-nerve discussions) reserved when laboratories talk about more definite partial block. Duration matters: if the proximal waveform is much broader, some of the amplitude loss is phase cancellation, not true block. Published consensus statements differ by nerve, by whether they use amplitude or area, and by how much duration increase they allow. Do not memorize a fake unpublished AAET official cutoff. State the idea: abnormal drop across a segment, distal CMAP relatively preserved, criteria vary, mimics exist.

Common mimics of block:

• Submaximal proximal stimulation. The proximal site is deeper (elbow, axilla, Erb's point, knee). If you have not reached a supramaximal plateau, the proximal CMAP is small for technical reasons.
• Co-stimulation. Distal stimulation of one nerve may be clean; proximal stimulation may spread into a neighbor, or the reverse, changing apparent amplitude.
• Anomalous innervation. A Martin-Gruber anastomosis can make ulnar stimulation at the wrist look larger than ulnar stimulation above the elbow in the same recording muscle, imitating ulnar forearm block.
• Temporal dispersion and phase cancellation. Desynchronized motor-unit action potentials cancel at the peak even though area falls less.
• Recording off the motor point, excess tissue, or a cold limb changing shape.

Neurapraxia is the traumatic version of focal demyelinating block: axons intact, no Wallerian degeneration, distal CMAP preserved after days, proximal stimulation across the lesion small or absent. Prognosis is relatively good once myelin and nodal function recover — a preview of the next section's injury grades.

If both proximal and distal CMAPs are 1 mV, you do not have conduction block as the main story. You have a small generator (axonal loss, muscle atrophy, or a distal lesion). Block requires a relatively preserved distal response.

Temporal dispersion

Temporal dispersion is desynchronization of the compound volley. Marked features:

• Increased duration of the negative phase
• Polyphasicity (extra turns and phases)
• Peak amplitude falls more than area, because opposite-polarity phases from late motor units cancel at the peak while the integral still counts those units

Dispersion is the electrical signature of unequal slowing among axons, typical of acquired demyelinating neuropathies and of very long irregular pathways. It is not a synonym for conduction block. A dispersed proximal CMAP can look small without a true all-or-none failure of many axons. Area comparison is the technologist's first screen: small and broad with relatively conserved area leans toward dispersion and cancellation; small and still compact with collapsed area leans toward block or axonal loss of contributing tissue.

SNAP dispersion is harder to mark because SNAPs are small and already brief, but a broad, low SNAP after a long proximal sensory path is the same physiology. Filter settings that round peaks can fake extra duration; match the laboratory's method before you call pathologic dispersion.

Demyelination as a family of findings

Demyelination (myelin or paranodal failure) produces some combination of:

• Prolonged distal latency
• Slow conduction velocity
• Conduction block
• Temporal dispersion
• Prolonged late responses (F waves), when those studies are performed

Not every demyelinated nerve shows block. Uniform demyelination, as in many Charcot–Marie–Tooth demyelinating phenotypes, may slow velocity diffusely with relatively less block and less dispersion than acquired inflammatory demyelination. Acquired inflammatory demyelination (chronic inflammatory demyelinating polyneuropathy (CIDP) and related disorders) is more likely to show multifocal slowing, block, and dispersion. Do not call a nerve demyelinated from a 2 m/s dip inside laboratory error, and do not call it axonal from a mildly small CMAP without looking at distal amplitude, velocity, and the opposite limb.

Diffuse processes versus multifocal disorders

A diffuse process affects nerves in a widespread, typically symmetric or length-dependent pattern. Examples:

• Length-dependent axonal polyneuropathy (distal SNAP and CMAP loss, relatively preserved velocity of remaining fibers) — the amplitude story continues in the next section
• Diffuse demyelinating polyneuropathy (CIDP-spectrum or inherited demyelinating neuropathy): many segments slow, distal latencies prolong, F waves prolong, dispersion may be widespread

A multifocal disorder hits named sites or named nerves in a patchy map:

• Multifocal motor neuropathy (MMN): persistent motor conduction block in non-entrapment segments, often upper limb, SNAPs typically spared, weakness in named-nerve distributions
• Mononeuritis multiplex (often axonal, vasculitic): stepwise named-nerve axonal loss
• Hereditary neuropathy with liability to pressure palsies (HNPP): recurrent focal block or slowing at common entrapment sites

CIDP versus MMN is a high-yield contrast. CIDP is a sensorimotor, often symmetric, proximal-and-distal demyelinating polyneuropathy. MMN is motor-predominant, asymmetric or multifocal, with motor block and relatively spared sensory studies. Treating them as the same electrical picture is an exam error. A single cubital-tunnel-style block in an otherwise normal study is an entrapment, not MMN by itself.

Focal slowing versus conduction block versus axonal loss

Worked waveform scenario

A motor study is supramaximal at both sites, G1 is on the motor point, and temperature is adequate.

• Distal CMAP amplitude = 8 mV, compact duration
• Proximal CMAP amplitude = 1 mV, no increase in duration, no extra phases
• Negative-peak area falls in proportion to amplitude

Amplitude drop = (8 − 1) / 8 = 87.5%. Duration did not explode, so phase cancellation is a poor explanation. Distal 8 mV says muscle and distal axons are largely present. The volley is failing between the two cathodes. That is conduction block across the tested segment until proven to be a technical mimic (submaximal proximal stimulus, co-stimulation, anomalous innervation). It is not distal axonal loss (that would have shrunk the 8 mV). It is not temporal dispersion as the main explanation (that would have broadened the proximal waveform and conserved area relative to the peak).

If instead the proximal CMAP were 4 mV and 18 ms long while the distal CMAP were 8 mV and 6 ms long, you would describe temporal dispersion and be cautious about calling block from amplitude alone.

Independent OpenExamPrep study of III.A.1.b.1–5 and 7 is this habit: name the spatial pattern (focal, multifocal, diffuse), then name the electrical behavior (slowing, block, dispersion, or — next — axonal loss), and refuse a fake official cutoff when the literature itself uses several.