Ulnar Nerve Palsy

Definition. Ulnar nerve palsy is compression or injury of the ulnar nerve, producing intrinsic muscle weakness and sensory loss. The ulnar nerve is the nerve of fine movement and power grip, and its loss is devastating for manual dexterity.

Where. The cubital tunnel at the elbow is the most common site of compression, and cubital tunnel syndrome is the second most common compression neuropathy. Guyon's canal at the wrist is the other site, and telling the two apart is the first task at the bedside.

The course. In the arm the nerve descends medial to the brachial artery and pierces the medial intermuscular septum at the arcade of Struthers. At the elbow it passes behind the medial epicondyle through the cubital tunnel, then enters the forearm between the two heads of flexor carpi ulnaris under Osborne's ligament. It runs deep to FCU through the forearm and enters Guyon's canal at the wrist, superficial to the flexor retinaculum. Knowing the course aids exposure.

The dorsal cutaneous branch. It leaves the nerve about 5 cm proximal to the wrist, before the nerve reaches Guyon's canal. That makes it the key to telling a high lesion from a low one.

Guyon's canal. The canal lies between the pisiform and the hook of hamate, which forms its lateral wall. The volar carpal ligament is the roof and the transverse carpal ligament the floor, and within it the nerve lies ulnar (medial) to the ulnar artery. The motor and sensory branches divide inside the canal, which gives it three zones:

• Zone 1 (proximal) - motor and sensory fibres; compression gives mixed symptoms
• Zone 2 (deep) - the motor branch only; compression gives a motor-only deficit (hook of hamate fracture)
• Zone 3 (superficial) - the sensory branch only; compression gives sensory symptoms only

The nerve in the canal may be compressed by a ganglion, a fracture or an ulnar artery aneurysm, and zone 2 is the most common site for ganglion cysts.

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What it supplies. In the forearm, FCU and the FDP to the ring and little fingers. In the hand the deep branch supplies the hypothenar muscles (ADM, FDM and ODM), all the palmar and dorsal interossei, the third and fourth lumbricals, adductor pollicis and the deep head of flexor pollicis brevis. The superficial branch is sensory, through the palmar digital nerves to the little finger and the medial half of the ring finger.

Median-ulnar communications. Anomalous cross-innervation between the median and ulnar nerves is common and a classic exam trap. It explains "atypical" deficits and false localisation on nerve conduction studies.

The Martin-Gruber anastomosis is a motor communication in the forearm, present in roughly 15 to 20 percent of limbs, in which fibres destined for ulnar-innervated intrinsics run in the median nerve (or its anterior interosseous branch) and cross over to join the ulnar nerve distally. A high (elbow) ulnar lesion may then spare more intrinsic function than expected, because those fibres bypass the lesion within the median nerve. On nerve conduction studies it can produce a spuriously high elbow-to-wrist amplitude or an initial positive deflection that mislocalises the block.

The Riche-Cannieu anastomosis is a communication in the hand between the deep (motor) branch of the ulnar nerve and the recurrent (motor) branch of the median nerve. With a large one the thenar muscles can be substantially ulnar-supplied (the "all-ulnar hand"), so a median nerve lesion spares thenar function. The converse "all-median hand" leaves the ulnar intrinsics working despite an ulnar lesion.

The cubital tunnel. This is the most common site. The nerve lies between the medial epicondyle and the olecranon under a roof formed by Osborne's ligament. Elbow flexion stretches it, and traction and compression combine to cause the injury.

Where it is caught at the elbow. Decompression releases five sites:

• Arcade of Struthers, 8 cm proximal
• Medial intermuscular septum
• Osborne's ligament, the roof of the cubital tunnel
• Arcade of Osborne, between the two heads of FCU
• Deep flexor-pronator aponeurosis

Compression. External pressure reduces intraneural blood flow. The large myelinated fibres are affected first, sensory before motor. Prolonged compression causes axonal degeneration, and Schwann cell damage leads to demyelination.

Traction. The nerve elongates with elbow flexion, and cubital tunnel pressure increases 6-fold in flexion. Chronic traction leads to fibrosis and adhesions.

Double crush. Compression at one site sensitises the nerve to compression at another, and cervical radiculopathy may coexist with cubital tunnel syndrome. Always examine the entire upper limb.

Progression. Seddon's classification applies:

• Neurapraxia - demyelination; complete recovery is expected
• Axonotmesis - axon damage; recovery depends on the distance to the target
• Neurotmesis - complete disruption; requires repair

McGowan grades cubital tunnel syndrome by the deficit:

• Grade I (mild) - sensory symptoms only (intermittent paraesthesia), no weakness
• Grade II (moderate) - weakness of the intrinsics and constant numbness; wasting may be present
• Grade III (severe) - profound weakness, severe wasting, paralysis

Dellon's classification is similar but adds objective sensory testing (two-point discrimination). Its staging is more precise for research, and the modification helps track recovery.

High or low. Localise the lesion before treating it.

The ulnar paradox. A high lesion claws less than a low one, and examiners love asking why it looks "better". The FDP to the ring and little fingers is paralysed as well, which removes the deforming flexor force at the IP joints. In a low lesion the profundus is intact and the clawing is severe.

The claw (Duchenne's sign). The ring and little fingers sit with the MCP joints hyperextended and the IP joints flexed. The ulnar-innervated medial two lumbricals and the interossei normally flex the MCP joints and extend the IP joints. Without them EDC hyperextends the MCP joints unopposed, and FDP and FDS flex the IP joints with no lumbrical anti-gravity force to resist them. The index and middle fingers are spared because their lumbricals are median-innervated.

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Examine for a pattern. Severe ulnar palsy is diagnosed from a pattern. Compare both hands for first dorsal interosseous and hypothenar wasting, look for persistent abduction of the little finger, test finger abduction against resistance, then assess key pinch.

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The named signs. Each points to the ulnar-innervated muscle that has failed:

• Froment's sign tests adductor pollicis. The patient holds a sheet of paper in a key pinch between the thumb and the side of the index finger; if the thumb IP joint flexes, flexor pollicis longus (median nerve) is compensating for a weak adductor.
• Jeanne's sign is hyperextension of the thumb MCP joint during the same pinch, from weakness of the deep head of FPB.
• Wartenberg's sign is persistent abduction of the little finger. The third palmar interosseous is too weak to adduct it, and EDM pulls it into abduction unopposed.
• Duchenne's sign is the claw.

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Provocative tests. The signs above confirm intrinsic weakness. Provocative manoeuvres localise the entrapment to the elbow, and together they form the OSCE battery for cubital tunnel syndrome:

• Tinel's sign - percussion over the nerve behind the medial epicondyle reproduces tingling in the ulnar digits. Sensitive but not specific: it is positive in many asymptomatic elbows.
• Elbow flexion test - the elbow is held in full flexion with the wrist in neutral or extension; paraesthesia in the ulnar distribution within about 30 to 60 seconds is positive. Flexion stretches the nerve and raises the pressure in the tunnel.
• Combined flexion-compression test - direct digital pressure just proximal to the cubital tunnel during elbow flexion is more sensitive than either manoeuvre alone.
• Scratch collapse test - with the patient resisting bilateral shoulder external rotation, a transient loss of resistance after the examiner lightly scratches the skin over the cubital tunnel is positive and helps localise the level.

Always reassess for dynamic subluxation of the nerve over the medial epicondyle during flexion, and screen the neck (C8/T1) and Guyon's canal to exclude a more proximal or distal cause.

Nerve conduction studies. What to look for:

• Slowing - conduction velocity less than 50 m/s across the elbow
• Conduction block - a drop in amplitude across the elbow of more than 20%
• EMG - denervation potentials in the ulnar-innervated muscles

Doing and reading the study. Record from ADM or FDI and stimulate above and below the elbow, measuring the distance carefully. Interpret velocity together with amplitude and needle EMG: slowing localises demyelination, whereas a reduced CMAP and denervation indicate axonal loss and a worse motor prognosis.

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Ultrasound. It can show nerve swelling, a cross-sectional area greater than 10 mm², best measured at the medial epicondyle by tracing inside the hyperechoic epineurial rim. It also identifies focal lesions and, during elbow flexion, dynamic subluxation, findings that can alter the operative plan.

How far to trust it. At the 10 mm² cut-off the pooled sensitivity is about 0.85 and the specificity about 0.91. Those figures come from studies comparing patients with healthy volunteers rather than with the conditions that actually mimic the syndrome, so an area above 10 mm² argues for the diagnosis while a normal scan does not exclude it.

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MRI. It is not required for every cubital tunnel syndrome. On MR neurography the affected nerve is enlarged and T2-hyperintense, with loss of its normal fascicular pattern. Use it when:

• the level is uncertain
• a mass or space-occupying lesion is suspected, such as a tumour or a ganglion in Guyon's canal
• trauma has distorted the anatomy
• denervation and alternative proximal pathology must be mapped

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The classic trap is mistaking a more proximal lesion for a focal ulnar entrapment.

The decision. Mild, sensory-only disease (McGowan grade I) gets a trial of conservative care. Motor involvement (grades II and III), or failure of conservative care, is the indication for surgery. Simple in-situ decompression is the evidence-based default, and transposition is reserved for frank instability, prior trauma, valgus deformity or revision.

Why decompression is the default. Bartels' randomised trial and subsequent meta-analyses show equivalent clinical outcomes with fewer complications after simple decompression, even when the nerve subluxes. Many surgeons still transpose a subluxating nerve, some because of concern about iatrogenic instability.

Algorithm

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Conservative care. The regimen:

• Night splinting with the elbow in 45° of flexion, which prevents maximal stretch
• Avoiding prolonged flexion, such as during phone use
• Nerve gliding exercises
• Patient education, which is key

Splinting and nerve gliding help mild disease, with success in roughly 50% of mild cases. Compliance is poor, however, and high-quality randomised evidence is limited.

In-situ decompression. For grade I or II disease with a static nerve, one that does not sublux. The release runs from 8 cm proximal (Struthers) to 6 cm distal (FCU) and frees all five sites. It is simple and preserves the nerve's vascularity, but has a higher recurrence. The other objection raised against it is failure if the nerve subluxes, although in Bartels' trial subluxation did not influence the outcome of simple decompression.

Anterior transposition. The nerve goes into one of two beds:

• Subcutaneous - the nerve is placed in the fat layer. There is a risk of hypersensitivity, and gentle handling is required.
• Submuscular - the nerve is buried deep to the flexor-pronator mass. Best for thin patients and recurrence.

Revision. Recurrence after simple decompression forces a decision: redo the decompression if the problem is adhesions, or transpose if the nerve subluxes. Submuscular transposition is the gold standard for revision, and most surgeons choose it.

MABC neuroma. The medial antebrachial cutaneous nerve crosses the field in the cubital tunnel approach and is often mistaken for a vein. Injury is common if the incision is too anterior and causes a painful neuroma with numbness over the olecranon. Find the nerve and protect it.

Pain is not always recurrence. A painful medial elbow after cubital tunnel surgery is not always recurrent ulnar compression. Ultrasound can show focal enlargement of an injured posterior MABCN branch adjacent to the ulnar nerve. Localise the maximal Tinel, map the sensory territory and use a diagnostic block before neuroma excision, repair or targeted reinnervation.

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Iatrogenic instability. A decompressed nerve can develop a new subluxation, snapping over the epicondyle with flexion. It requires revision transposition, and submuscular transposition solves it.

Proximal kinking. Failure to release the medial intermuscular septum or the arcade of Struthers during transposition creates a new compression point. Always release the proximal and distal fascia.

Outcome. Results are good for grades I and II. In grade III, recovery of the intrinsics is unpredictable and often incomplete.

Patient factors. Older patients recover less motor function, and diabetes is a poor prognostic factor (a "double crush").

Global Epidemiology

• Cubital tunnel syndrome (ulnar neuropathy at the elbow) is the 2nd most common upper-limb compression neuropathy after carpal tunnel syndrome.
• Population-based incidence: roughly 20 to 25 per 100,000 person-years (Siena, Italy cohort), with a clear male predominance and rising incidence with age.
• Strong association with manual/occupational elbow flexion and leaning, and with diabetes, smoking and prior elbow trauma/valgus deformity.

Side-by-Side Guideline Comparison

Practice Variation: High vs Limited Resource Settings

• High-resource: Routine access to NCS/EMG, high-resolution ultrasound, and endoscopic release; nerve transfers (SETS AIN-to-ulnar) available in tertiary hand units.
• Limited-resource: Diagnosis often clinical without electrodiagnostics; open simple decompression is the mainstay due to low cost and minimal equipment; tendon transfers for fixed claw deliver high value where microsurgical reconstruction is unavailable.
• Therapy: Skilled hand therapists for 'anti-claw' (lumbrical-bar) splinting and nerve-gliding programmes substantially improve outcomes and are emphasised across all settings.

Endoscopic or open release. Symptom relief is equivalent. Endoscopic release offers less scar tenderness but a higher haematoma rate, and there is no clear winner.

Subcutaneous or submuscular transposition. There is no high-level evidence that either is superior. The choice is driven by soft-tissue cover and surgeon preference.

Nerve transfer (SETS). Promising for high and severe lesions, but the evidence is largely retrospective and outcomes are strongly time-dependent, better with surgery under 12 months. Counsel that the evidence is evolving and recovery remains variable.