16.1 Radiculopathy, Root Avulsion, and Sensory Neuronopathy

Why root and ganglion geography still belong on the NCS worksheet

Outline topics VI.B.2 (dorsal-root ganglion / sensory neuronopathies) and VI.B.3 (root disease: radiculopathy, polyradiculopathy, root avulsion) ask the same electrical question Chapter 7 introduced anatomically: is the peripheral sensory axon still attached to its dorsal-root ganglion (DRG)? Independent OpenExamPrep teaching for Registered Nerve Conduction Study Technologist (R.NCS.T.) candidates treats radiculopathy, avulsion, and neuronopathy as three different answers to that question, not as three nicknames for a small compound muscle action potential (CMAP). This is independent study material that follows published outline headings. It is not an official American Association of Electrodiagnostic Technologists (AAET) course and does not claim partnership with the certifying body.

Needle electromyography (EMG) of paraspinals and a myotomal muscle map is physician interpretation. The technologist still has to record the sensory nerve action potentials (SNAPs), CMAPs, F waves, and H-reflexes that make a root-versus-plexus-versus-ganglion argument possible. A worksheet that only shows a low extensor digitorum brevis CMAP has not finished the job.

Anatomy the worksheet actually uses

Each spinal segment sends a ventral (motor) root from anterior-horn cells and a dorsal (sensory) root into the DRG. The sensory neuron is pseudounipolar: one process runs centrally through the dorsal root into the cord; the other runs peripherally through spinal nerve, plexus, and named nerve. The DRG nourishes both processes.

In typical teaching anatomy the DRG sits in the intervertebral foramen. Compression inside the spinal canal (posterolateral disc, stenosis, osteophyte) often injures the root proximal to or at the root proper while leaving the ganglion and its peripheral sensory process in continuity. That is why standard electrodiagnostic teaching says SNAPs are typically spared in radiculopathy. The patient can still have radiating pain and dermatomal numbness because the central process or the root is blocked or irritable; conscious sensation is not the same thing as a recordable SNAP.

A far-lateral / extraforaminal disc or a lesion that invades the foramen can injure the DRG itself. That exception drops SNAPs and must sit on the same page as the rule. Do not treat one missing sural SNAP in an older foot as proof that the lesion is postganglionic plexus disease.

Paraspinal muscles are supplied by the dorsal ramus, which leaves near the spinal nerve. Physician needle EMG of paraspinals can support a lesion at or proximal to that takeoff. Pure plexopathy, distal to dorsal-ramus branching, typically spares paraspinals. That needle map is not an R.NCS.T. procedure, but it is why a complete SNAP panel still matters: you are building the pre- versus postganglionic case the interpreting physician will finish.

Radiculopathy: the everyday root lesion

Radiculopathy is root injury, most often compressive (disc herniation, foraminal stenosis, spondylosis) and sometimes inflammatory or infiltrative. The electrical pattern after enough time for Wallerian degeneration of any disconnected motor axons is:

• SNAPs typically present in the corresponding cutaneous nerve, because the peripheral sensory axon remains connected to the DRG.
• CMAPs may fall if enough ventral-root axons are lost in that myotome. A modest single-root lesion often leaves CMAPs normal because muscles have overlapping root supply. Severe C8–T1, L5, or S1 axonal radiculopathy can shrink abductor pollicis brevis (APB), extensor digitorum brevis (EDB), or abductor hallucis (AH) CMAPs.
• Conduction velocity of remaining fibers is not demyelinating-polyneuropathy slow. You do not diagnose L5 radiculopathy by a 20 m/s fibular velocity.
• F waves travel through the ventral root, but they also travel through several roots that co-innervate the recorded muscle. A single-level radiculopathy often leaves F-wave latency normal. Absent or very prolonged F waves in one nerve are more persuasive when the lesion is polyradicular, hyperacute and proximal, or when that muscle is heavily dependent on one root.
• The soleus H-reflex is an S1-weighted monosynaptic loop (Ia afferents through the DRG and dorsal root, then motor axons out the ventral root). An abnormal H-reflex with a spared sural SNAP is classic teaching for S1 radiculopathy rather than a postganglionic tibial or sciatic sensory lesion. The H-reflex is not a private S1 test — polyneuropathy and neuronopathy also degrade it — but in a unilateral radiating-pain case it is a high-yield late response.

Pain and a dermatomal sensory complaint with spared SNAPs is not a machine error. It is the preganglionic sensory story. If you skip sensory NCS because “the patient is numb anyway,” you throw away the localization.

Worked myotomal CMAP examples (teaching, not unpublished official cut scores)

These are classroom localizers, not AAET numeric thresholds:

• C6–C7 radiculopathy: median SNAP to the long finger typically spared; a low biceps or triceps CMAP appears only if axonal motor loss is substantial.
• C8–T1 radiculopathy: ulnar and medial antebrachial cutaneous (MABC) SNAPs typically spared (those axons’ DRGs are intact); APB and abductor digiti minimi CMAPs may fall together in a myotomal pattern, unlike a single median or ulnar mononeuropathy.
• L5 radiculopathy: superficial fibular SNAP typically spared; EDB CMAP may fall; this is the NCS contrast with fibular neuropathy at the fibular head, where the superficial fibular SNAP can drop (Chapter 14).
• S1 radiculopathy: sural SNAP typically spared; AH CMAP may fall; soleus H-reflex often abnormal on the symptomatic side.

Polyradiculopathy

Polyradiculopathy means multiple roots, not a single disc at one level. Teaching settings include cauda equina compression, cytomegalovirus lumbosacral polyradiculopathy (especially in profound immunocompromise), leptomeningeal metastasis, inflammatory polyradiculitis, and some diabetic or infectious radiculoplexus attacks that behave electrically like multi-root disease.

NCS expectations:

• If the process remains root-level and DRGs survive, SNAPs may still be spared even when several myotomes are weak.
• Several CMAPs can be low after motor Wallerian time.
• F waves become more informative than in single-root disease: multiple motor roots in the loop are compromised, so F-wave absence or marked delay in more than one nerve is a proximal-motor clue.
• H-reflexes can be bilaterally poor if S1 roots are included.

If SNAPs are also widely gone, do not force a pure-root story. Add sensory neuronopathy, polyneuropathy, plexopathy, or combined root-and-nerve disease to the differential. Polyradiculopathy is a map of how many roots, not a license to ignore sensory amplitudes.

Root avulsion

Root avulsion is a traumatic preganglionic tear of rootlets from the cord, classically in high-energy brachial-plexus trauma (motorcycle, traction). Dorsal rootlets avulsed proximal to the DRG leave the ganglion and the peripheral sensory axon in continuity. After Wallerian time those SNAPs can remain present even in an anesthetic dermatome. Ventral rootlets avulsed from anterior-horn cells disconnect motor axons, which then degenerate, so the CMAP may fall.

Typical electrodiagnostic teaching clocks (classroom ranges, not unpublished official AAET cut scores): motor amplitudes often change over about 3–7 days; sensory amplitudes often lag, up to about 7–11 days. A SNAP recorded on day 0 does not yet prove preganglionic injury. A SNAP that is still present after the sensory Wallerian window, in a numb territory, is the avulsion-supporting pattern.

Late responses:

• F waves need an intact ventral-root / anterior-horn loop. Avulsed motor roots yield absent or unobtainable F waves in that myotome once the pathway is interrupted.
• H-reflexes need Ia afferents through the dorsal root and DRG into the cord, then motor outflow. Dorsal-root avulsion abolishes the H-reflex even when the peripheral sensory axon — and therefore the SNAP — still lives.

That SNAP-present / late-response-absent combination is the worksheet’s version of “the cable to the limb is alive; the cable into the cord is not.”

Combined pre- and postganglionic injury is common. An absent SNAP does not exclude avulsion; it means there is also postganglionic sensory axon loss, a recording of the wrong nerve, or a study performed before postganglionic axons have degenerated. Postganglionic plexus rupture (Chapter 15) drops the relevant SNAPs. The SNAP panel (lateral antebrachial cutaneous, median digital, ulnar digital, MABC, and the matching CMAPs) is how you separate those maps, not a single APB millivolt.

Sensory neuronopathy (ganglionopathy)

Sensory neuronopathy (also called ganglionopathy) destroys DRG cell bodies. Peripheral sensory axons then degenerate because they have lost their somata. Electrical pattern:

• SNAPs low or absent, often non-length-dependent: upper-limb SNAPs can fall as much as or more than sural SNAPs; proximal cutaneous nerves can fail along with digital nerves. That is the opposite of a distal dying-back polyneuropathy that attacks the toes first.
• Motor NCS relatively spared (CMAPs and motor velocities not the main story). Mild motor abnormalities can appear if the disease is not purely sensory or if disuse and concurrent illness intervene, but a neuronopathy worksheet should not look like mixed sensorimotor axonal polyneuropathy.
• H-reflexes are poor, because the Ia afferent cell bodies live in the DRG.
• F waves, which are motor loops, may remain obtainable if anterior-horn cells and ventral roots are intact — another contrast with radiculopathy or avulsion that interrupts motor roots.

Clinical frame: sensory ataxia, pseudoathetosis of the fingers, and numbness that does not respect a distal-stocking gradient. Teaching associations include paraneoplastic sensory neuronopathy (anti-Hu / ANNA-1, often with small-cell lung cancer), Sjögren ganglionopathy, platinum chemotherapy, high-dose pyridoxine (vitamin B6) toxicity, some infectious and immune ganglionopathies, and idiopathic cases. The electrical signature is widespread SNAP loss that does not behave like diabetic distal polyneuropathy.

SNAP / CMAP / late-response localization table

Typical electrodiagnostic teaching after Wallerian time has passed. These are pattern descriptions, not unpublished official AAET cut scores.

Case 1 — Lumbar radiculopathy versus lumbosacral plexopathy

A 54-year-old has acute left posterolateral leg pain after a lift, foot drop, and reduced pinprick on the dorsum of the foot. Superficial fibular and sural SNAPs are present and symmetric after more than 10 days. Left EDB CMAP is low; tibial CMAPs are nearer to the opposite side. Left soleus H-reflex is present (S1 loop intact). Independent OpenExamPrep reading: spared SNAPs argue against a postganglionic lumbosacral plexopathy or a fibular neuropathy at the fibular head as the full explanation. The map fits an L5-predominant radiculopathy. If this had been plexopathy, the superficial fibular SNAP (and often other plexus-routed SNAPs) would be at risk of falling. If it had been fibular-head neuropathy, look for focal slowing or block across the fibular head and a vulnerable superficial fibular SNAP.

Case 2 — Paraneoplastic sensory neuronopathy

A 62-year-old smoker develops subacute sensory ataxia in the hands and feet over weeks, with little true weakness. Median, ulnar, radial, and sural SNAPs are all absent or barely recordable. CMAPs and motor velocities are relatively preserved. H-reflexes are unobtainable. F waves are still present. This is not length-dependent diabetic polyneuropathy (the hands would not match the feet this early, and motor axons usually join a mixed axonal neuropathy). It is a non-length-dependent SNAP wipeout with spared motor NCS — sensory neuronopathy. The technologist’s job is a complete SNAP panel, including nerves that distal-polyneuropathy protocols sometimes skip. The physician pursues paraneoplastic and immune evaluation; NCS does not name the antibody.

Case 3 — Traumatic avulsion

A motorcyclist has a flail C5–C6 arm and a numb thumb. Ten days later, the lateral antebrachial cutaneous SNAP and median SNAP to the thumb are present. Biceps and deltoid CMAPs are low. F waves from those myotomes are absent. Independent OpenExamPrep reading: preserved SNAPs after the sensory Wallerian window support preganglionic avulsion rather than isolated postganglionic upper-trunk axonal loss (which would drop those SNAPs). If the same SNAPs had been absent, you would describe postganglionic (or combined) injury, not a pure avulsion pattern. Do not call the present SNAP a laboratory error because the patient cannot feel the dermatome.

What the technologist must still do

Record the cutaneous nerves that belong to the myotome in question. Wait, or at least date, the study relative to injury. Add H-reflexes when S1 is in the story and F waves when the question is proximal motor continuity. Temperature, distances, and side-to-side comparisons remain the usual technical rules. Independent OpenExamPrep study of VI.B.2–3 is this habit: SNAP geography first, then CMAP and late responses, then the clinical frame — radiculopathy, polyradiculopathy, avulsion, or ganglionopathy — without inventing unpublished official cut scores.