EDX · EP 06 · ELECTRODIAGNOSTICS
Before You Listen
- Prerequisites: the four phases of needle electromyography (EMG) and the patterns of acute and chronic denervation from EDX-05; basic spinal nerve anatomy (root, dorsal root ganglion, ventral and dorsal primary rami, plexus formation); the H-reflex and F-wave physiology covered in EDX-04; and familiarity with the cervical and lumbosacral myotomes and dermatomes.
- Runtime: 1 hour 6 minutes.
- Topic in one line: the dorsal root ganglion (DRG) principle that keeps sensory nerve action potentials (SNAPs) normal in radiculopathy despite clinical sensory loss; the cervical (C5 to T1) and lumbosacral (L2 to S1) myotomes anchored on dual-innervated muscles (deltoid + infraspinatus for C5, brachioradialis + pronator teres for C6, triceps + flexor carpi radialis for C7, first dorsal interosseous + flexor pollicis longus for C8, vastus medialis + tibialis anterior for L4, tibialis anterior + tibialis posterior for L5, medial gastrocnemius + gluteus maximus for S1); the chronological evolution of EMG findings from reduced recruitment (days) through paraspinal fibrillations (7-10 days) to distal limb fibrillations (3-6 weeks); the H-reflex as the most sensitive test for S1 radiculopathy; the HI MADAM mnemonic; and the three-feature radiculopathy-vs-plexopathy table (SNAPs, paraspinals, distribution).
Vignette. A 45-year-old man presents with three weeks of progressive right foot drop. He reports lateral leg numbness and difficulty clearing his great toe when walking. Nerve conduction studies (NCS) show a normal right superficial fibular sensory nerve action potential (SNAP) and a normal sural SNAP. Needle EMG shows 2+ fibrillation potentials and positive sharp waves (PSWs) in the tibialis anterior (deep fibular nerve), peroneus longus (superficial fibular nerve), tibialis posterior (tibial nerve), and tensor fasciae latae (superior gluteal nerve). Lumbar paraspinals show 2+ fibrillations.
What is the diagnosis, why is the SNAP normal despite clinical sensory loss, which single muscle in this stem distinguishes the diagnosis from a common fibular neuropathy at the fibular head, and what additional muscle would distinguish a sciatic neuropathy from a fibular neuropathy at the knee?
(Answer at the end of this chapter)
Section 1: The Dorsal Root Ganglion Principle
Bottom line: the dorsal root ganglion (DRG) sits in the intervertebral foramen outside the spinal canal; in radiculopathy the lesion is proximal to the DRG, so the peripheral sensory axon stays in continuity with its cell body, no Wallerian degeneration occurs, and the sensory nerve action potential (SNAP) is preserved despite clinical numbness; this normal-SNAP-with-clinical-sensory-loss is the single most important distinction between radiculopathy and plexopathy on the boards.
The dorsal root ganglion (DRG) principle is the single most important concept in the electrodiagnostic evaluation of radiculopathy. It explains why sensory nerve action potentials (SNAPs) remain normal in radiculopathy despite clinical sensory deficits.
The DRG is located in the intervertebral foramen, outside the spinal canal in most cervical and lumbar levels. It contains the cell bodies of primary sensory neurons. The peripheral process extends distally through the plexus and peripheral nerve to the sensory receptor; the central process extends proximally through the dorsal root into the spinal cord.
In radiculopathy, the nerve root is compressed or injured proximal to the DRG (within the spinal canal or at the foraminal entrance). Because the DRG cell body is intact and the peripheral sensory axon remains in continuity with its cell body, Wallerian degeneration does not occur in the peripheral sensory nerve. The sensory axon continues to conduct normally, and the SNAP remains normal.
The patient may experience significant sensory symptoms (numbness, tingling, burning pain) in the dermatome of the affected root. These arise from dysfunction at the root level, disrupting sensory signal transmission into the spinal cord, but the peripheral sensory nerve is physiologically intact and the SNAP is preserved. The combination of normal SNAPs plus abnormal needle EMG in a myotomal distribution is the electrodiagnostic signature of radiculopathy. If the SNAP is abnormal in the territory of the clinical deficit, the lesion is at or distal to the DRG; the differential expands to plexopathy or peripheral neuropathy.
Several scenarios complicate the DRG principle. Concurrent peripheral neuropathy is a common challenge: diabetic polyneuropathy may produce abnormal SNAPs unrelated to the radiculopathy. The L5 DRG sits within or very near the intervertebral foramen and in some individuals may be intraspinal; a large L4-L5 disc could damage the L5 DRG directly, producing an abnormal superficial fibular SNAP in what is otherwise a root-level lesion. The S1 DRG may also sit more proximally than other lumbar levels.
Five governing principles. First, radiculopathy cannot be diagnosed by NCS alone; needle EMG must be performed. Second, the study must be timed appropriately. Third, a sufficient number of muscles must be examined, including paraspinals and muscles from different peripheral nerves sharing the suspected root. Fourth, the SNAP is expected to be normal in pure radiculopathy. Fifth, EMG detects only the motor axon loss component; purely sensory or demyelinating radiculopathies may produce normal EMG findings. The sensitivity of EMG for radiculopathy is approximately 50 to 85% for cervical and somewhat higher for lumbosacral, depending on protocol and timing.
Source: Henry Vandyke Carter, “Gray’s Anatomy plate 799”, via Wikimedia Commons, Public Domain. https://commons.wikimedia.org/wiki/File:Gray799.svg
High Yield — DRG principle and the radiculopathy signature
- DRG location: intervertebral foramen, outside spinal canal in most cervical and lumbar levels.
- Radiculopathy = preganglionic lesion (proximal to DRG). Sensory cell body intact, peripheral axon does not degenerate, SNAP normal despite clinical numbness.
- Plexopathy and peripheral neuropathy = postganglionic (distal to DRG). SNAP abnormal (Wallerian degeneration of peripheral sensory axon).
- Radiculopathy electrodiagnostic signature: normal SNAPs + abnormal needle EMG in a myotomal distribution.
- L5 DRG exception: sometimes intraspinal, large disc herniation may damage the DRG directly and produce an abnormal superficial fibular SNAP.
- EMG sensitivity: ~50-85% for cervical radiculopathy, somewhat higher lumbosacral. Timing-dependent. EMG detects only motor axon loss; pure sensory or demyelinating radiculopathies yield normal EMG.
Mnemonic — “Pre-ganglionic preserves the SNAP”
The DRG is the sensory cell body. Preganglionic = root-level (radiculopathy) = SNAP preserved. Postganglionic = plexus or peripheral nerve = SNAP lost. If a stem describes clinical numbness with a normal SNAP, the answer is radiculopathy. If the SNAP is abnormal, the answer is plexopathy or peripheral neuropathy.
And then it hits the herniated disc. The signal is physically blocked from entering the spinal cord. The brain never receives the message. So the patient truly feels numbness. When we test the peripheral nerve in the clinic, the sensory nerve action potential is robust.
— EDX-06 podcast, ~08:00