Paresis Nervus Radialis

01Pathophysiology

The radial nerve originates from the posterior cord of the brachial plexus, carrying fibers from nerve roots C5 through T1. After leaving the axilla, the nerve wraps posteriorly around the humeral shaft within a bony channel known as the spiral (radial) groove. This fixed anatomical relationship is the single most important concept to understand: the nerve is tethered against bone, making it extremely vulnerable to injury whenever the humeral shaft is fractured, compressed, or subjected to traction.

Above the elbow, the radial nerve innervates the triceps (elbow extension), brachioradialis (forearm flexion in neutral), extensor carpi radialis longus (ECRL), and anconeus. These branches typically depart proximal to or at the level of the spiral groove, which is why a lesion at the groove itself usually spares the triceps but abolishes wrist and finger extension.

As the nerve crosses the lateral epicondyle and enters the forearm, it divides into two terminal branches. The posterior interosseous nerve (PIN) is the deep, purely motor branch that passes beneath the fibrous arch of the supinator muscle (the arcade of Frohse) and innervates all remaining wrist and finger extensors: extensor carpi radialis brevis, supinator, extensor digitorum communis, extensor carpi ulnaris, extensor digiti minimi, abductor pollicis longus, extensor pollicis longus, extensor pollicis brevis, and extensor indicis. The superficial branch is a purely sensory nerve supplying the dorsal aspect of the hand over the first web space and radial three and a half digits (proximal phalanges only).

This branching pattern directly explains the clinical presentations. A lesion at the spiral groove produces both motor loss (wrist drop and finger drop) and sensory loss (dorsal hand). An isolated PIN lesion produces finger drop without complete wrist drop, because the ECRL (innervated above the split) is preserved, and there is no sensory deficit because the superficial branch remains intact. The fact that the PIN is a pure motor nerve and the superficial branch is a pure sensory nerve is heavily tested.

Wrist drop occurs because the extensor carpi radialis brevis and extensor carpi ulnaris are paralyzed, eliminating active wrist extension. The resulting flexed wrist position weakens the grip because the finger flexors cannot generate optimal tension without a stable, extended wrist. This phenomenon is often tested as "apparent grip weakness" that normalizes when the examiner passively extends the patient's wrist, a finding that confirms the lesion is in the radial nerve and not in the median or ulnar nerve.

02Classification and Clinical Manifestation

By Level of Injury

By Nerve Injury Severity

03Diagnostic Workup

The diagnosis of radial nerve palsy is fundamentally clinical. A patient presenting with wrist drop, finger drop at the MCP joints, and sensory loss over the first dorsal web space after a humeral fracture or prolonged compression should be diagnosed at the bedside. The examination must systematically test individual muscles to localize the level: ask the patient to extend the elbow against resistance (triceps, C7), flex the forearm in neutral position (brachioradialis, C5-C6), extend the wrist (ECRL/ECRB, C6-C7), extend the fingers at the MCP joints (extensor digitorum, C7-C8), and extend the thumb (extensor pollicis longus, C7-C8). Also test the brachioradialis reflex and check sensation on the dorsum of the first web space.

Plain radiographs should be obtained immediately when trauma is involved. A mid-shaft or distal-third humeral fracture (the Holstein-Lewis fracture pattern) carries the highest association with radial nerve injury because the nerve is most tightly adherent to the bone at this level.

EMG and nerve conduction studies are the confirmatory test, but the timing is critical. They must not be performed before 3 weeks post-injury because Wallerian degeneration has not yet progressed distally. If done too early, fibrillation potentials and positive sharp waves will not yet be detectable in denervated muscles, producing a falsely reassuring study. NCS can localize a conduction block at the spiral groove, and the superficial radial sensory nerve action potential (SNAP) will be reduced or absent in lesions proximal to the sensory branch takeoff.

When a pure PIN syndrome presents without trauma, MRI of the proximal forearm is indicated to evaluate for a compressive mass (lipoma, ganglion, or synovial proliferation at the arcade of Frohse). Ultrasound is increasingly used as a dynamic, real-time tool to visualize nerve continuity, caliber changes, and extrinsic lesions.

04Management & Treatment

Acute stabilization centers on the wrist splint. A dynamic or static cock-up splint positions the wrist in 30 to 45 degrees of extension and the MCP joints in slight flexion, restoring the mechanical advantage of the finger flexors and allowing functional grip during recovery. Passive range-of-motion exercises for the wrist and fingers should begin immediately to prevent joint stiffness and tendon adhesions. Occupational therapy referral is standard.

For the vast majority of closed injuries (Saturday night palsy, neuropraxia from a humeral fracture managed conservatively), the nerve recovers spontaneously. The expected timeline is 6 to 12 weeks for neuropraxia and several months for axonotmesis, with regeneration occurring at approximately 1 mm per day from the site of injury.

The critical decision point on the exam is: when do you operate? The answer is that a closed injury is observed for 3 to 4 months with serial clinical and electrodiagnostic monitoring. If there is no sign of reinnervation (no voluntary motor unit potentials in the most proximal radial-innervated muscle distal to the lesion), surgical exploration is indicated. Conversely, an open injury with nerve deficit at presentation demands early surgical exploration, because the likelihood of nerve transection is high and delay worsens outcomes.

A radial nerve palsy that develops after manipulation or closed reduction of a humeral fracture (i.e., the palsy was not present before the procedure and appeared afterward) is a red flag for nerve entrapment in the fracture fragments. This situation calls for urgent surgical exploration to free the trapped nerve.

Tendon transfers are the salvage procedure for irreversible palsy. The classic triple transfer (pronator teres to ECRB, FCU to EDC, PL to rerouted EPL) is a well-tested concept. The key exam point is that tendon transfers require supple joints (no contractures) and a functioning donor muscle, which is why passive range of motion must be maintained from the outset.

05Differential Diagnosis & Distractors

06Traps & High-Yield Pearls

The most common way students lose points on radial nerve palsy questions falls into three categories.

First, confusing the level of injury with the expected motor deficit. A vignette describing a mid-shaft humeral fracture with wrist drop but preserved triceps function should immediately localize to the spiral groove. Students who see "wrist drop + humeral fracture" and select "high radial nerve injury" will incorrectly predict triceps weakness that the vignette does not describe. The exam is testing whether you understand the sequential branching of the nerve and can match the deficit pattern to the anatomical level.

Second, misidentifying PIN syndrome. A question may describe isolated finger drop with radial deviation of the wrist on attempted extension and no sensory loss. Students who answer "radial nerve palsy at the spiral groove" will be wrong because a spiral groove lesion always produces sensory loss over the dorsal hand and complete (not partial) wrist drop. The absence of sensory loss is the single fastest way to distinguish PIN syndrome from a higher lesion.

Third, ordering electrodiagnostic studies too early. A vignette presenting a patient 5 days after a humeral fracture with wrist drop and asking for the "next best step" is testing whether you know that EMG/NCS performed before 3 weeks will yield unreliable results. The correct next step at that stage is clinical observation and wrist splinting, not electrodiagnostic testing.

The overarching competency being assessed is anatomical localization of a peripheral nerve lesion. The exam expects you to: (1) identify the nerve involved from the motor and sensory deficit pattern, (2) determine the level of the lesion along that nerve based on which muscles are spared and which are affected, (3) select the appropriate timing for confirmatory studies, and (4) know the indications for observation versus surgical intervention based on the mechanism (open vs. closed) and the recovery timeline.