Paresis Nervus Ulnaris

01Pathophysiology

The ulnar nerve arises from the C8 and T1 nerve roots via the medial cord of the brachial plexus. It descends along the medial arm, then passes through a fibro-osseous tunnel at the elbow called the cubital tunnel, located directly posterior to the medial epicondyle. This is where the nerve is most vulnerable because it is superficial, tethered, and subject to both traction (during elbow flexion) and direct compression (when leaning on the elbow). The cubital tunnel is the most common site of ulnar nerve entrapment and the second most common upper extremity compressive neuropathy overall, after carpal tunnel syndrome.

Distally, the nerve enters the hand through Guyon's canal, a space bounded by the pisiform bone and the hook of the hamate, covered by the volar carpal ligament. Compression here is less common but classically associated with cycling (handlebar palsy), ganglion cysts, or hook of hamate fractures.

Understanding the nerve's motor and sensory distribution explains the clinical findings. In the forearm, the ulnar nerve innervates the flexor carpi ulnaris (FCU) and the medial half of the flexor digitorum profundus (FDP) (to the ring and little fingers). In the hand, it innervates the hypothenar muscles, all interossei (dorsal and palmar), the 3rd and 4th lumbricals, the adductor pollicis, and the palmaris brevis.

The claw hand deformity is the hallmark motor finding. The lumbricals normally flex the MCP joints and extend the IP joints. When the 3rd and 4th lumbricals are paralyzed, the unopposed extensor digitorum communis (radial nerve) hyperextends the MCP joints, while the intact FDP flexes the DIP joints, producing the "claw" posture of the ring and little fingers. This leads to one of the most tested concepts: the ulnar paradox. In a high lesion (at or above the elbow), the FDP to the ring and little fingers is also paralyzed, so the DIP joints cannot flex, and the claw is less pronounced. In a low lesion (at the wrist), the FDP is intact, so the DIP flexion component is preserved, and the claw is more pronounced. In other words, the more distal the injury, the worse the deformity. This is counterintuitive and heavily tested.

Froment's sign reflects loss of the adductor pollicis. When the patient is asked to pinch a sheet of paper between the thumb and index finger, they cannot adduct the thumb and instead compensate by flexing the thumb IP joint using the flexor pollicis longus (median nerve). The examiner sees thumb IP flexion rather than a straight-thumb pinch.

Wartenberg's sign is persistent abduction of the little finger at rest. The 3rd palmar interosseous muscle (which normally adducts the 5th digit) is paralyzed, leaving the extensor digiti minimi (radial nerve) unopposed.

Sensory loss follows a predictable pattern: the palmar and dorsal surfaces of the medial 1.5 fingers (the little finger and the ulnar half of the ring finger). In Guyon's canal lesions, the dorsal sensation may be spared because the dorsal cutaneous branch of the ulnar nerve branches off proximal to the wrist and does not travel through Guyon's canal. This distinction is a reliable localizing clue on exam.

02Classification and Clinical Manifestation

By Site of Lesion

Guyon's Canal Zones

McGowan Classification

03Diagnostic Workup

The workup begins with a thorough clinical examination. Two provocation tests are commonly used for cubital tunnel syndrome. The Tinel's sign at the elbow involves tapping the ulnar nerve behind the medial epicondyle; reproduction of tingling into the ring and little fingers is positive. The elbow flexion test involves sustained maximal elbow flexion with wrist extension for 60 seconds; reproduction of paresthesias is positive and has greater sensitivity than Tinel's alone.

For wrist-level lesions, palpation over Guyon's canal may reproduce symptoms. A palpable mass raises suspicion for ganglion cyst.

The best initial confirmatory test is electrodiagnostic study (NCS and EMG combined). This is the gold standard workup for peripheral nerve entrapment and serves dual purposes: confirming the diagnosis and localizing the lesion. On NCS, the hallmark finding is a decrease in motor conduction velocity across the elbow to below 50 m/s, or a velocity drop of more than 10 m/s compared to the forearm segment. Sensory nerve action potentials (SNAPs) of the dorsal cutaneous branch help distinguish elbow from wrist lesions: if the dorsal cutaneous SNAP is abnormal, the lesion is at or above the elbow. EMG showing fibrillation potentials and positive sharp waves in the first dorsal interosseous and abductor digiti minimi confirms active denervation.

Imaging is adjunctive. Plain radiographs of the elbow are ordered when there is a history of trauma or when cubitus valgus deformity is suspected ("tardy ulnar palsy" from a remote lateral condyle fracture in childhood). Wrist radiographs including a carpal tunnel view help identify hook of hamate fractures. MRI is reserved for suspected soft tissue mass, failed conservative treatment, or atypical presentations. High-resolution ultrasound is increasingly used as a quick, non-invasive tool to measure nerve cross-sectional area and identify subluxation over the medial epicondyle during dynamic elbow flexion.

04Management and Treatment

Conservative Management

For mild and early moderate cases, conservative treatment is first-line and should be maintained for at least 3 to 6 months before considering surgery.

Activity modification is the cornerstone. The patient is instructed to avoid prolonged elbow flexion, leaning on the elbow, and repetitive flexion-extension activities. For cyclists with handlebar palsy, padded gloves and handlebar adjustment are recommended.

Nocturnal splinting of the elbow at approximately 30 to 45 degrees of flexion (not full extension, which is uncomfortable, but enough to prevent sustained flexion) reduces traction on the nerve. A simple towel wrap around the elbow at night can serve the same purpose.

NSAIDs such as ibuprofen 400 to 600 mg three times daily or naproxen 250 to 500 mg twice daily are used for short-term symptom relief during flares.

Nerve gliding exercises, performed under the guidance of a hand therapist, improve nerve excursion within the cubital tunnel and are supported by moderate evidence for symptom improvement.

Corticosteroid injection at the cubital tunnel is generally not recommended due to the superficial location of the nerve and the risk of direct nerve injury. This is a point of distinction from carpal tunnel syndrome, where injection is a standard conservative option.

Surgical Management

Surgery is indicated when conservative management fails after 3 to 6 months, when there is progressive motor weakness, muscle atrophy, or when electrodiagnostic studies show worsening denervation.

For cubital tunnel syndrome, three main procedures exist:

In situ decompression (simple release of the cubital tunnel retinaculum) is the least invasive and preferred for patients without nerve subluxation. Recovery is faster, but it does not address subluxation.

Anterior transposition moves the nerve from behind the medial epicondyle to an anterior position. This can be subcutaneous (under skin and fat), intramuscular (within the flexor-pronator mass), or submuscular (deep to the flexor-pronator origin). Submuscular transposition is the most protective and is often chosen for revision surgery or severe cases, but it requires a longer rehabilitation.

Medial epicondylectomy removes a portion of the medial epicondyle to eliminate the bony prominence compressing the nerve. It is used less frequently today.

For Guyon's canal syndrome, the treatment is surgical decompression of the canal, often combined with excision of the offending lesion (ganglion cyst, anomalous muscle). Hook of hamate fractures that compress the nerve require excision of the hook fragment.

Postoperative Rehabilitation

Early protected range of motion begins within the first week. Strengthening exercises are introduced at 4 to 6 weeks. Full recovery of motor function may take 3 to 6 months in moderate cases and up to 12 to 18 months in severe cases. Patients with significant preoperative atrophy may have incomplete motor recovery.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The single most commonly tested trap with ulnar nerve palsy is the ulnar paradox. A vignette may describe a patient with a severe claw hand deformity and ask you to localize the lesion. The instinct is to assume the more dramatic deformity corresponds to a more proximal or more severe lesion. That instinct is wrong. A more pronounced claw hand points to a distal (wrist-level) lesion because the FDP is intact, allowing full DIP flexion. A proximal (elbow-level) lesion paradoxically produces a less dramatic claw because the FDP is also paralyzed. If the vignette describes "loss of wrist flexion toward the ulnar side" (FCU weakness) or "inability to flex the DIP joints of the ring and little fingers" (FDP involvement), these point to a high lesion.

Another common pitfall is confusing Froment's sign with intrinsic hand weakness from other causes. Froment's sign is about compensatory thumb IP flexion during a lateral pinch task. It is not simply "weak grip." The test isolates adductor pollicis function and is the single most reliable bedside sign for ulnar motor involvement in the hand.

A third trap involves sensory localization. If the vignette states that the patient has numbness on the palmar side of the little finger but normal sensation on the dorsum of the hand, this points to a lesion at Guyon's canal, not the cubital tunnel. The dorsal cutaneous branch leaves the ulnar nerve well proximal to the wrist and is spared in wrist-level lesions. The absence or presence of dorsal sensory loss is often the single detail that separates a correct from an incorrect answer.

Finally, watch for the "tardy ulnar nerve palsy" vignette. The patient is typically an older adult with a history of a childhood elbow fracture (lateral condyle fracture leading to non-union, subsequent cubitus valgus deformity). The ulnar nerve is progressively stretched over years, and the patient presents decades later with insidious hand weakness. The delayed onset after a remote fracture is the giveaway.

The core competency being tested across all these question formats is your ability to localize a peripheral nerve lesion using motor deficits, sensory distribution, and provocation tests, and then to match that localization to the correct clinical decision (conservative versus surgical management and timing).