Radiculopathy vs Peripheral Nerve Lesion

Telling a radiculopathy from a peripheral nerve entrapment is one of the most commonly tested localisation problems in orthopaedic and neurology examinations, and the cost of getting it wrong is concrete: the wrong investigation (MRI of the spine versus nerve conduction studies) and the wrong treatment, a decompression at the wrong site. What follows is a structured approach built on dermatomal mapping, reflex examination and electrodiagnostic correlation.

The classic confusions. Each pair shares a presenting complaint and parts company on examination:

• Cervical radiculopathy and carpal tunnel syndrome both cause hand tingling; mislocalise and the injection or the operation goes to the wrong site
• Lumbar radiculopathy and peroneal neuropathy both cause foot drop; the surgical target differs
• C5 radiculopathy and axillary neuropathy both weaken the deltoid; the MRI is requested at the wrong level
• Root avulsion and brachial plexus injury differ fundamentally in prognosis and surgical planning

How common. Cervical radiculopathy has an annual incidence of approximately 83 per 100,000, and C7 is the root most often affected. Lumbar radiculopathy has a lifetime prevalence of around 1-5%, most commonly at L5 and S1. On the peripheral side, carpal tunnel syndrome is the most common entrapment, the median nerve at the wrist, with a prevalence of approximately 3-6%; peroneal neuropathy is the most common lower limb mononeuropathy, usually at the fibular neck.

The dorsal root ganglion. The DRG sits within the intervertebral foramen, and where a lesion lies relative to it decides what the sensory nerve conduction study will show. A preganglionic lesion, root compression inside the spinal canal proximal to the DRG, leaves the sensory cell body intact, so the distal sensory axon survives and the sensory nerve action potential (SNAP) remains normal despite clinical sensory loss. A postganglionic lesion, in the plexus or a peripheral nerve distal to the DRG, disconnects the sensory axon from its cell body; Wallerian degeneration follows and the SNAP is reduced or absent. This is the single most important electrophysiological discriminator between radiculopathy and a plexus or peripheral nerve lesion.

Dorsal and ventral root. The dorsal root carries sensation, and its compression gives dermatomal pain, paraesthesia and numbness in a band. The ventral root carries the motor fibres, and its compression gives myotomal weakness, fasciculations and eventually atrophy. Clinical radiculopathy usually involves both, a mixed sensorimotor picture, but isolated motor or sensory radiculopathy can occur.

Wallerian degeneration runs to a timetable:

• Days 0-3: the axon is discontinuous but the distal segment still conducts, so NCS may be normal
• Days 7-10: the distal axon begins to degenerate
• Days 14-21: Wallerian degeneration is complete; CMAP and SNAP amplitudes drop in peripheral nerve lesions

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The question at the bedside is which of three levels the lesion sits at, root, plexus or peripheral nerve, and each has a signature in the pattern of sensory loss, the pattern of weakness and the reflexes.

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Dermatome or territory. Each spinal root supplies a band of skin, its dermatome. Adjacent dermatomes overlap, which is why a single-root lesion rarely gives complete anaesthesia. Several roots recombine in the plexus to form each named peripheral nerve, so a peripheral nerve's cutaneous territory is a discrete area that does not follow the dermatomal bands. Sensory loss that crosses a peripheral nerve boundary should therefore make you think of root or plexus; sensory loss confined to a named territory points to the nerve.

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History. A root lesion gives neck or back pain radiating into the limb, worse with extension or Valsalva, with tingling in a dermatomal pattern. A peripheral nerve gives numbness in a specific territory with positional provocation, elbow flexion for the ulnar nerve for instance, and nocturnal symptoms in carpal tunnel. A plexus lesion brings severe limb pain, a history of trauma or radiation exposure, a mass in the supraclavicular or axillary region, and symptoms across more than one territory.

Examination asks four questions, in order:

1. Map the sensory loss. Draw the area of numbness on the patient and compare it with the dermatome and peripheral territory maps: a band or a named territory?
2. Test individual muscles. Which are weak and which are strong, and does the pattern cross nerve boundaries? Myotomal means root.
3. Check the reflexes. A lost reflex localises the root level.
4. Provoke. Spurling for a cervical root, straight leg raise for a lumbar root, Tinel and Phalen for a peripheral nerve (Tinel is elicited over the nerve itself), Adson for the thoracic outlet.

Reflexes are the fastest bedside localisation tool because they are root-specific. A lost reflex narrows the root level; if the reflex is intact the root is likely not severely compressed, though a mild radiculopathy can spare reflexes. Most reflexes are polysegmental, which is why a peripheral nerve lesion usually leaves them intact. Proximal to the table below, hip flexion (iliopsoas) tests L2/L3 and knee extension (quadriceps) L3/L4.

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First line. The examination above: the sensory map, muscle-by-muscle testing, the reflexes and the provocative tests. Electrodiagnostic studies are the second line, and imaging follows.

Timing of EMG. Fibrillation potentials take 10-21 days to develop, so wait at least 3-4 weeks after onset. Before Wallerian degeneration is complete, under 3 weeks, the EMG may be normal or show only reduced recruitment without fibrillations, and a falsely reassuring study is the most common exam trap.

Needle EMG shows fibrillations and positive sharp waves in denervated muscle. Which muscles carry them, and whether the paraspinals do, is what localises: paraspinal involvement means radiculopathy, and the distribution across a root versus a peripheral nerve pattern clinches the diagnosis.

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The late responses. The standard battery interrogates the distal nerve and the muscle; the F-wave and the H-reflex sample the proximal segment and the root, the very region a radiculopathy lives in.

F-wave. A late muscle response produced when the stimulus travels antidromically up the motor axon to the anterior horn cell and back down, so it tests the whole motor pathway including the proximal root. In radiculopathy the F-wave latency may be prolonged, or the F-wave may show reduced persistence or chronodispersion, but F-waves are non-specific: they sample many roots, so a single-root lesion is often diluted, and they are most useful for diffuse processes such as Guillain-Barre.

H-reflex. The electrophysiological equivalent of the ankle (Achilles) reflex, a true monosynaptic reflex (Ia afferent to alpha motor neuron) recorded from soleus/gastrocnemius after tibial nerve stimulation. It is the single best NCS for the S1 root: a prolonged or absent H-reflex, compared side to side, is an early, sensitive sign of S1 radiculopathy, and unlike needle EMG it is abnormal immediately, without waiting the three weeks for fibrillations. Its limitations are that it is non-localising (an S1 lesion anywhere along the arc abolishes it), it cannot be repeated reliably once abolished, and it normally disappears with age or peripheral neuropathy.

Imaging. MRI of the cervical or lumbar spine for a suspected radiculopathy looks for disc herniation, foraminal stenosis and root compression. A weak structural correlate, a small protrusion without meaningful root or canal compression, should prompt examination and testing for an extraspinal peripheral lesion rather than automatic attribution to the spine. MRI of the brachial plexus for a suspected plexus lesion looks for tumour, traumatic injury and inflammation. For a suspected entrapment, ultrasound or MRI of the peripheral nerve finds the structural cause: a ganglion, a lipoma, a fibrous band.

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Double crush. A nerve compressed at one site becomes more susceptible to compression at a second site along its course, because axoplasmic transport is impaired. Clinically the patient may have both a C6/C7 radiculopathy and carpal tunnel syndrome, and both may need treatment; metabolic neuropathy (diabetes) and multiple entrapment points are the risk factors. Consider proximal and distal compression sites whenever the clinical picture does not fit a single localisation, address both, and treat the more accessible one first.

What predicts recovery. The best prognosis belongs to an acute presentation with a short duration of symptoms, a partial rather than complete lesion, a distal entrapment site, a younger patient and no comorbid neuropathy. The poor prognostic factors are the mirror image:

• Root avulsion (preganglionic)
• Complete axonal loss on EMG
• Duration over 12 months before intervention
• A proximal lesion, with a longer regeneration distance
• Diabetes or another neuropathy

The window. Muscles must be reinnervated within 12-18 months. After that the motor end plates degenerate irreversibly and tendon transfers become the only option.