Curriculum/Pillar 5 · Clinical Electrodiagnostics

Plexopathies

Module 20 of 36·28 min read

Learning objectives

1Map abnormalities onto brachial and lumbosacral plexus anatomy
2Separate plexopathy from radiculopathy and mononeuropathy electrically
3Recognise the special patterns of traumatic and neuralgic plexopathy

The plexus is where the simple parallel bundles of the nerve roots are rewoven into the named peripheral nerves, and a plexopathy is therefore a lesion of that weave. Its diagnosis rests on one electrical fact that distinguishes it cleanly from its commonest mimic: the plexus lies distal to the dorsal root ganglion, so a plexopathy is a postganglionic lesion and the sensory nerve action potentials are reduced or absent. Everything else is anatomy applied to that single separator.

Brachial plexus architecture

The brachial plexus runs roots → trunks → divisions → cords → terminal branches (the mnemonic Robert Taylor Drinks Cold Beer). The C5–C6 roots merge into the upper trunk, C7 continues as the middle trunk, and C8–T1 form the lower trunk. Each trunk splits into anterior and posterior divisions; the posterior divisions of all three trunks unite into the posterior cord (radial and axillary nerves), the anterior divisions of the upper and middle trunks form the lateral cord (musculocutaneous and the lateral head of the median), and the anterior division of the lower trunk continues as the medial cord (ulnar and the medial head of the median). This topology is the key to localisation, because each level predicts a characteristic combination of nerves involved across different roots.

Upper trunk / Erb's point (C5–C6).The classic traction injury (the “waiter's tip” posture): weakness of deltoid, biceps, brachioradialis, and supraspinatus/ infraspinatus, with a reduced lateral antebrachial cutaneous SNAP. Spans the axillary, musculocutaneous, and suprascapular nerves — different nerves, common trunk.
Lower trunk / Klumpke (C8–T1). An intrinsic-hand failure affecting both median- and ulnar-innervated thenar and hypothenar muscles, with reduced ulnar and medial antebrachial cutaneous SNAPs. A Horner syndrome implicates the T1 ventral ramus and raises concern for a very proximal (often malignant) process.
Cords. A lateral-cord lesion weakens the musculocutaneous-supplied biceps and the median-supplied forearm flexors while sparing ulnar muscles; a posterior-cord lesion produces a radial-plus-axillary deficit; a medial-cord lesion mimics combined ulnar and lower-median involvement.

The root-versus-plexus electrical logic

A radiculopathy is preganglionic — the lesion is proximal to the DRG, so the peripheral sensory axon survives and the SNAP is preserved despite dermatomal numbness. A plexopathy is postganglionic — distal to the DRG, so Wallerian degeneration of the peripheral sensory axon makes the SNAP reduced or absent. This is the decisive separation: numb arm with a normal SNAP points above the ganglion (root); numb arm with a low or absent SNAP points at or below it (plexus or nerve). Paraspinal denervation, supplied by the dorsal ramus proximal to the plexus, should be absent in a pure plexopathy — its presence reopens the question of a root lesion or a combined root-and-plexus process.

The lumbosacral plexus

The lumbar plexus (L2–L4) lies within the psoas and gives rise to the femoral and obturator nerves; the sacral plexus (L4–S3) forms the sciatic, superior and inferior gluteal, and pudendal nerves. Localising studies use the saphenous SNAP for the femoral/lumbar territory and the sural and superficial peroneal SNAPs for the sciatic/sacral territory; their reduction confirms a postganglionic lesion and separates a lumbosacral plexopathy from an L-level radiculopathy with a preserved SNAP. The same trunk/cord logic applies: a lesion that crosses the territory of more than one named nerve while remaining confined to one plexus division identifies the level.

Traumatic patterns and the avulsion exception

Most plexopathies are traumatic, typically from traction (motorcycle injuries stretching the upper trunk, or a downward arm pull tearing the lower trunk). The general postganglionic rule has one critical exception: a root avulsion tears the rootletsproximal to the DRG, so the peripheral sensory axon stays in continuity with its cell body and the SNAP is paradoxically preserved despite a profound, anaesthetic, and flail limb. The combination of a clinically dense sensory loss with a normal SNAP and denervated paraspinals is the electrodiagnostic signature of avulsion — a finding with major surgical and prognostic weight, because an avulsed root cannot be repaired distally.

Common Pitfall

A normal SNAP does not always mean “not a plexus problem.” In severe traction injuries, intraspinal root avulsion leaves the peripheral sensory neuron intact and the SNAP normal even though the limb is anaesthetic and flail — a preganglionic lesion masking as preserved. Reading that normal SNAP as reassurance, rather than as evidence of avulsion, inverts the prognosis. Pair every SNAP with the paraspinal needle exam and the clinical sensory deficit before concluding.

Neuralgic amyotrophy and the radiation-versus-tumour problem

Neuralgic amyotrophy (Parsonage–Turner syndrome) is an idiopathic, presumed immune-mediated, often post-viral or post- vaccination brachial plexopathy that announces itself with severe shoulder-girdle pain for days to weeks, followed by patchy weakness and atrophy as the pain subsides. It favours the upper trunk and individual nerves (characteristically the long thoracic, suprascapular, and anterior interosseous), producing a multifocal, often partial axonal pattern rather than a clean trunk lesion. Prognosis is generally favourable but recovery takes months to years.

In the patient with prior malignancy, the central question is radiation plexopathy versus neoplastic infiltration, and the needle exam supplies the most specific discriminator. Myokymic discharges — grouped, rhythmically recurring motor unit potentials firing in bursts — are strongly associated with radiation-induced plexopathy and are uncommon in tumour. Radiation plexopathy also tends to be painless, upper-trunk predominant, and slowly progressive, often after a latency of months to years and after doses above roughly 60 Gy. Neoplastic infiltration is typically painful, lower-trunk predominant (the axillary apex), and frequently accompanied by a Horner syndrome. Finding myokymia tips the balance decisively toward radiation; its absence with pain and lower-trunk involvement should prompt imaging for recurrence.

Clinical Pearl

The SNAP is the workhorse that separates the plexus from the root. Before you call a plexopathy, confirm that the sensory response in the suspect territory is reduced or absent (postganglionic) and that the paraspinals are normal — then localise by finding weakness that crosses several named nerves but stays within one trunk, division, or cord. If the SNAP is instead preserved with a numb limb, you are above the ganglion: either a radiculopathy or, in the traumatic setting, a root avulsion.

Key points

Roots → trunks → divisions → cords → branches: upper trunk = Erb/C5–C6 (waiter's tip), lower trunk = Klumpke/C8–T1 (intrinsic hand ± Horner).
Plexopathy is postganglionic, so SNAPs are REDUCED/ABSENT — the key electrical separator from a radiculopathy, which preserves the SNAP.
Paraspinals (dorsal ramus, proximal to the plexus) should be normal in a pure plexopathy; their involvement reopens a root lesion.
Root avulsion is the exception: preganglionic tear preserves the SNAP despite a flail, anaesthetic limb — a major surgical/prognostic flag.
Myokymic discharges favour radiation plexopathy (painless, upper-trunk); painful, lower-trunk, Horner-associated disease suggests neoplastic infiltration.