Curriculum/Pillar 1 · Electrophysiology of Motor Systems

Electrical Signal Generation

Module 2 of 36·30 min readLIVE MODEL
Learning objectives
  • 1Trace the genesis of the MUAP, CMAP, and SNAP from single-fibre potentials
  • 2Explain temporal and spatial summation and volume conduction
  • 3Connect recruitment and rate coding to the recorded interference pattern

The waveforms on the screen are not the action potentials themselves; they are voltages that those potentials project through the conducting volume of the body to a distant electrode. Mastering electrodiagnosis means thinking in two layers at once — the all-or-none membrane events at the source, and the smoothed, summed, distance-weighted potential field they create at the recording site. This chapter derives every signal you measure, from the single-fibre spike to the CMAP and the microvolt SNAP, from the physics of summation and volume conduction.

From single fibres to the motor unit potential

A needle in muscle does not record one fibre; it records the algebraic sum of the action potentials of every fibre of the nearest motor unit that lies within its pickup volume. Because the fibres of one unit are scattered across a 5–10 mm territory and the conduction velocity along each fibre differs slightly, their individual spikes arrive at the electrode at marginally different times. The recorded motor unit action potential (MUAP) is therefore a temporal summation of asynchronous single-fibre potentials, and its features map directly onto this geometry:

  • Amplitude is dominated by the few fibres nearest the electrode tip, because extracellular potential falls off steeply with distance. Amplitude is thus a local measure and varies wildly with needle position over millimetres.
  • Duration reflects the temporal spread of arrivals across the whole unit and therefore samples a larger fibre population; it is the most reliable index of motor-unit territory and the quantity that lengthens in chronic reinnervation.
  • Phases and turns index the synchrony of firing. Loss of synchrony — from variable reinnervated conduction times or from fibre splitting — produces the polyphasia (> 4 phases) seen in both neurogenic and myopathic remodelling.
Near versus far: the inverse-distance rule

In a volume conductor the extracellular potential of a fibre falls steeply with radial distance — sharp, high-frequency spikes attenuate fastest, while slow components persist. A fibre 0.5 mm from the electrode can dominate the trace; one a few millimetres away contributes only a rounded, low-frequency hum. This is why MUAP amplitude is treated as a near-field property and why we judge a recording "crisp" (sharp rise time, < 500 µs) before trusting its amplitude — a distant unit looks deceptively small and slow.

The waveform at the electrode: a moving dipole and the triphasic shape

To understand the shape of any propagating potential, picture the depolarized region of membrane as a moving electrical source. Ahead of the advancing front the membrane is at rest and the extracellular space is relatively positive; under the front it is intensely negative; behind it, repolarization restores positivity. To a stationary electrode that the impulse approaches, passes, and leaves, this travelling dipole reads as a triphasic waveform: an initial positive deflection, a large negative peak, and a terminal positive deflection — the canonical signature of a potential propagating past a recording point.

Two corollaries are clinically load-bearing. First, when the depolarization originates directly under the active electrode (as at the motor point, or with the active electrode optimally placed over the endplate zone for a CMAP), there is no initial positivity — the potential is biphasic with an initial negativity, and the negative onset marks the true latency. Second, this is why the recording convention matters: by agreement, negativity at the active electrode deflects the trace upward, so the dominant negative peak is the upward peak you measure.

The initial positivity is a localization clue

An unexpected initial positive deflection on a CMAP is not noise — it is information. It means the depolarization reached the active electrode from elsewhere: the electrode is off the motor point, or the response is volume-conducted from a co-stimulated neighbouring muscle. Either way the onset latency is corrupted, because you are timing the arrival of a travelling front rather than a local origin. Reposition before you measure.

Recruitment and rate coding: building the interference pattern

A single motor unit can grade its own tension only modestly by firing faster (rate coding); large increments of force require activating additional units (recruitment), and the two mechanisms operate together across the voluntary range. By Henneman's size principle, units are recruited in a fixed order of increasing size — small, fatigue-resistant type I units first, large type II units last — because small motor neurons have higher input resistance and reach threshold for less synaptic current. As more units fire and each fires faster, their MUAPs overlap on the screen into a dense, unresolvable interference pattern. Two quantitative readouts summarize the balance:

  • Recruitment frequency — the firing rate of the first unit at the moment a second unit appears (normally ~10 Hz). A first unit firing much faster than this before any second unit joins signals that too few units are available — reduced recruitment.
  • Recruitment ratio — the firing rate of the fastest unit divided by the number of active units (normally ≈ 5). A ratio well above 5 is the neurogenic pattern; an abnormally full screen at trivial force is the myopathic pattern.
LIVE MODELMotor unit recruitment and the interference pattern, live
motor unit pool — small → large (lit = recruited)
Units active
5/18
Mean firing rate
11Hz
Recruitment ratio
2.2
Pattern
Normal

Orderly small-to-large recruitment with balanced rate coding — a normal interference pattern.

Drive voluntary effort and watch single MUAPs sum into an interference pattern exactly as temporal and spatial summation predict. In Normal mode, units recruit small-to-large with a balanced ratio near 5. Switch to Neuropathic: few surviving units fire very fast yet the screen stays sparse — a high recruitment ratio, the picket fence you can count through. Switch to Myopathic: many small units flood the screen for almost no force — early (full) recruitment. These mirror-image abnormalities are the single most useful distinction made at the needle, and both preserve the recruitment order.

Temporal and spatial summation in the recorded field

The macroscopic signals of nerve conduction studies are governed by the same two summations, now applied across an entire population of axons or fibres firing in near-synchrony. Spatial summationis the superposition of many sources' fields at one electrode at one instant; temporal summation is the integration over time of arrivals that are slightly desynchronized. The critical consequence is that summation of asynchronous sources is lossy: when the constituent potentials are not perfectly aligned in time, the negative peaks of some coincide with the positive tails of others, and the summed amplitude is smaller than the arithmetic sum of individual peaks. This phase cancellation is the hidden mechanism behind several core phenomena and is most extreme in sensory recordings.

The CMAP: a summed, synchronized motor response

The compound muscle action potential (CMAP) is the summated electrical response of all the muscle fibres activated when a motor nerve is stimulated supramaximally. Because supramaximal stimulation recruits every axon and the resulting muscle spikes are tightly synchronized, the CMAP is large — typically several to > 10 mV — and its negative-peak amplitude (or area) is a quantitative surrogate for the number of functioning motor axons and fibres. Onset latency times the fastest-conducting motor axons plus neuromuscular transmission and a short muscle-activation delay. Two failure modes are diagnostic: uniform axon loss lowers amplitude with little change in shape, whereas demyelination between stimulation and recording sites desynchronizes arrivals, producing temporal dispersion (a broadened, lower, polyphasic CMAP) and, when current leak is severe enough, conduction block — a drop in amplitude and area across the affected segment.

The SNAP: why sensory responses are microvolt-scale

The sensory nerve action potential (SNAP) records the travelling potential of sensory axons directly, without the enormous amplifying relay of muscle. Three physical facts collapse its amplitude into the microvolt range (typically ~5–50 µV, versus the millivolt CMAP):

  • No muscle amplification — each motor axon commands hundreds of large muscle fibres, so the CMAP is a vastly amplified readout; the SNAP is the bare nerve signal with no such gain.
  • Phase cancellation over distance— sensory fibres span a range of conduction velocities, so the longer the conduction distance, the more the fast and slow fibres' biphasic potentials drift out of phase and cancel. SNAP amplitude therefore declines with recording distance, a normal, distance-dependent attenuation that is far more severe for the brief sensory spikes than for the broader CMAP.
  • Reference proximity — the active and reference electrodes sit only a few centimetres apart, so both record part of the same travelling potential; the SNAP is the small difference between two similar signals, magnifying its sensitivity to inter-electrode distance.

The practical upshot is that the SNAP is exquisitely vulnerable to background noise and demands averaging, meticulous impedance control, and standardized montage. Its great compensating virtue is localizing power: because the sensory cell body sits in the dorsal root ganglion distal to the root, a lesion proximal to the ganglion (a root avulsion or radiculopathy) leaves the peripheral sensory axon intact and the SNAP preserved, even when the dermatome is clinically numb — a discriminator examined in the localization chapters.

several–>10 mV
Typical CMAP amplitude
~5–50 µV
Typical SNAP amplitude
≈ 5
Normal recruitment ratio
~10 Hz
Recruitment frequency
Clinical Pearl
When a CMAP looks broad and small, decide whether you are seeing axon loss or desynchronization before you call it. Proximal-to-distal comparison settles it: pure axon loss drops amplitude proportionally at every stimulation site with a stable shape, whereas demyelination makes the proximal response progressively broader, lower, and more polyphasic than the distal one. The phase-cancellation physics that quietly shrinks every SNAP is the same physics that, when pathological, broadens the CMAP.
Common Pitfall
Do not read MUAP or CMAP amplitude as a fixed property of the patient. It is a near-field, position- and montage-dependent measurement: a unit recorded a few millimetres off, or an active electrode placed off the motor point, looks small and slow not because fibres are lost but because distance and phase cancellation have attenuated the signal. Optimize rise time and electrode position first; only then is amplitude interpretable, and only against electrode- and distance-matched normative data.
Key points
  • Recorded waveforms are volume-conducted potential fields, not the membrane spikes themselves — think source and field simultaneously.
  • A potential propagating past an electrode is triphasic (positive–negative–positive); one originating under the electrode is biphasic with initial negativity that marks true latency.
  • MUAP amplitude is a near-field property (nearest fibres dominate); duration samples the whole unit and best indexes territory and reinnervation.
  • Force is graded by recruitment (size principle, small→large) and rate coding; recruitment ratio ≈ 5, with reduced (neurogenic) and full (myopathic) being mirror images.
  • The CMAP is a large, synchronized, muscle-amplified summed response (mV); axon loss lowers amplitude, demyelination causes dispersion and block.
  • The SNAP is microvolt-scale because it lacks muscle amplification and suffers phase cancellation over distance; its DRG location preserves it in preganglionic root lesions.
Further reading
  1. 1.Preston DC, Shapiro BE. Electromyography and Neuromuscular Disorders. 4th ed. Elsevier; 2021: Ch. 3, 15.
  2. 2.Kimura J. Electrodiagnosis in Diseases of Nerve and Muscle. 4th ed. Oxford University Press; 2013: volume conduction and compound potentials.
  3. 3.Stålberg E, Trontelj JV, Sanders DB. Single Fiber EMG. 3rd ed. Edshagen; 2010: single-fibre potentials and summation.
  4. 4.Daube JR, Rubin DI. Needle electromyography. Muscle Nerve. 2009;39:244–270.
  5. 5.Dumitru D, Amato AA, Zwarts M. Electrodiagnostic Medicine. 2nd ed. Hanley & Belfus; 2002: generation of bioelectric potentials.
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