EDX · EP 01 · ELECTRODIAGNOSTICS
Before You Listen
Episode Setup
- Topic in one line: the cellular machinery that drives every nerve conduction study and needle electromyogram (EMG): the neuron, the action potential, the motor unit, saltatory conduction, the neuromuscular junction safety factor, the Henneman size principle, and the Wallerian degeneration timeline that determines when an electrodiagnostic (EDX) study can detect what.
- Prerequisites: undergraduate-level membrane physiology (resting potential, ion channels), basic peripheral neuroanatomy (nerve roots, plexus, peripheral nerves), and the principle that the dorsal root ganglion (DRG) lies outside the spinal cord.
- Runtime: 1 hour 8 minutes.
Vignette. A 47-year-old electrician sustains a deep laceration to the volar forearm during a workplace accident. He is taken to the emergency department, where the wound is irrigated and closed. He has dense numbness over the median nerve sensory distribution and cannot oppose the thumb. Three days later he is referred for an electrodiagnostic study to determine the severity of the median nerve injury. The electromyographer performs nerve conduction studies and notes that the median compound muscle action potential (CMAP) recorded from abductor pollicis brevis (APB) is still present with stimulation distal to the laceration, although already slightly reduced in amplitude. Needle examination of APB shows reduced recruitment but no fibrillation potentials.
What is the optimal timing of a comprehensive electrodiagnostic study after acute axonal nerve injury, what are the expected findings on day three versus week three, what cellular event explains why fibrillation potentials are absent on day three, and at what rate would regenerating axons travel from the laceration toward the thenar eminence if axonotmesis is confirmed?
(Answer at the end of this chapter)
Section 1: The Neuron, Axonal Transport, and the Dorsal Root Ganglion Principle
Bottom line: action potentials are initiated at the axon hillock because that segment carries the highest density of voltage-gated sodium channels and therefore the lowest firing threshold; the dorsal root ganglion (DRG) sits inside the intervertebral foramen, outside the spinal cord, which is why a radiculopathy never produces an abnormal sensory nerve action potential (SNAP) even when the patient is clinically numb; and the rate of slow axonal transport, roughly one to three millimeters per day, sets the speed limit on peripheral nerve regeneration.
The neuron is the fundamental signaling cell of the nervous system. Every peripheral motor and sensory neuron has three principal domains: the cell body (soma) houses the nucleus and the entire protein-synthesis machinery, including the rough endoplasmic reticulum (Nissl bodies) and a prominent Golgi apparatus; the dendrites are branching extensions that receive synaptic input; and the axon is a single elongated projection that conducts the action potential away from the soma toward its target.
The axon hillock sits at the junction between the soma and the proximal axon. It contains the highest density of voltage-gated sodium channels anywhere on the neuron, giving it the lowest threshold for firing, and every action potential begins there. When a board question asks where the action potential is initiated, the answer is always the axon hillock.
The axon depends entirely on the soma for protein synthesis. Fast anterograde transport, powered by kinesin motors along microtubules, carries vesicles, mitochondria, and membrane-associated proteins at approximately 200 to 400 mm per day. Slow anterograde transport carries cytoskeletal proteins such as neurofilaments and tubulin at only 0.5 to 5 mm per day. Retrograde transport, powered by dynein motors, returns degraded materials, endosomes, and neurotrophic factors at approximately 150 to 200 mm per day. The clinical payoff is the rate of slow axonal transport, roughly 1 to 3 mm per day, which limits the speed of peripheral nerve regeneration after axonal injury. This is the basis for the clinical estimate that reinnervation proceeds at approximately one inch per month (about 25 mm per month).
The DRG cell body of every sensory neuron lies outside the spinal cord, within the intervertebral foramen. This anatomical fact is the most powerful localization principle in electrodiagnostic medicine. In a radiculopathy, the pathology sits at the nerve root, proximal to the ganglion. Because the sensory cell body and its peripheral axon remain connected and intact, the distal sensory axon does not undergo Wallerian degeneration. Sensory nerve action potentials (SNAPs) remain normal in radiculopathy, even when the patient has clinical numbness in the affected dermatome. This is a preganglionic lesion. By contrast, in a plexopathy or peripheral neuropathy, the lesion sits distal to the ganglion: the sensory axon is separated from its cell body, Wallerian degeneration proceeds, and SNAPs become abnormal.
Myelin is the lipid-rich insulating sheath that wraps around axons and dramatically increases conduction velocity while conserving metabolic energy. In the peripheral nervous system (PNS), myelin is produced by Schwann cells with a strict one-to-one relationship: one Schwann cell wraps a single internode of a single axon. In the central nervous system (CNS), myelination is performed by oligodendrocytes, where a single oligodendrocyte can myelinate segments of up to 40 to 50 different axons simultaneously. Schwann cells also have a basement membrane (oligodendrocytes do not), and that basement membrane contributes to the robust regenerative capacity of peripheral nerves. Unmyelinated axons in the PNS are also associated with Schwann cells but are not individually wrapped; instead, multiple small-diameter unmyelinated axons sit within invaginations of a single Schwann cell, forming Remak bundles. The internode length, the distance between successive nodes of Ranvier, is proportional to axon diameter, typically about 100 times the axon diameter. Larger axons therefore have longer internodes and faster conduction. After regeneration, remyelinated fibers have shorter internodes than the original, producing permanently slower conduction velocity than the pre-injury baseline.
Source: Mysid (vectorized from Tristanb), “Spinal nerve”, via Wikimedia Commons, CC BY-SA 3.0. https://commons.wikimedia.org/wiki/File:Spinal_nerve.svg
High Yield — Neuron, transport, and the DRG rule
- Action potential initiation = axon hillock (highest voltage-gated Na+ channel density, lowest threshold).
- Axonal transport speeds: fast anterograde 200-400 mm/day (kinesin); slow anterograde 0.5-5 mm/day (cytoskeleton); retrograde 150-200 mm/day (dynein).
- Nerve regeneration rate = ~1-3 mm/day = ~1 inch/month, set by slow axonal transport.
- DRG sits in the intervertebral foramen (outside the cord). Radiculopathy = preganglionic = SNAP NORMAL even when patient is numb.
- Plexopathy / peripheral neuropathy = postganglionic = SNAP ABNORMAL.
- Schwann cell = 1 cell per 1 internode of 1 axon (PNS); oligodendrocyte = up to 40-50 axons (CNS).
- Remak bundle = multiple unmyelinated axons in one Schwann cell.
- Internode length ~100x axon diameter; remyelinated internodes are shorter → permanently slower CV.
Mnemonic — “Numb but normal” = preganglionic
If the stem says the patient is dense numb in a single dermatome but the SNAP from that territory is normal, the lesion is at or proximal to the dorsal root ganglion. That is a radiculopathy or a root avulsion. If the SNAP is abnormal in the same numb territory, the lesion is distal to the ganglion: plexopathy, peripheral neuropathy, or a postganglionic lesion.
You cannot rebuild a highway faster than the heavy freight trains can deliver the asphalt and the steel. So that one to three millimeters per day translates to a really handy clinical rule of thumb: re-innervation proceeds at approximately one inch, or 25 millimeters, per month.
— EDX-01 podcast, ~8:53