Ulnar nerve palsy is the loss of sensory and motor function. This can occur after injury to any portion of the ulnar nerve. The ulnar nerve is the terminal branch of the medial cord (C8, T1). The ulnar nerve innervates the flexor carpi ulnaris after it passes through the cubital tunnel.
Other muscles innervated by the ulnar nerve are the flexor digitorum profundus of the ring and small fingers and the following hand muscles:
When the ulnar nerve is injured, the muscles innervated by the nerve begin to weaken. This leads to an imbalance between the strong extrinsic muscles (i.e., extensor digitorum communis) and the weakened intrinsic muscles (i.e., interosseous and lumbricals). This imbalance is characterized clinically by metacarpophalangeal (MCP) hyperextension and proximal interphalangeal (PIP) and distal interphalangeal (DIP) flexion.
Causes of claw hand can also be due to anything that may lead to ulnar nerve palsy. Ulnar nerve palsy can arise from a laceration anywhere along its course. Proximal injuries to the medial cord of the brachial plexus may also present with sensory loss distally. Ulnar nerve palsies can also be due to cubital tunnel syndrome and ulnar tunnel syndrome. These are compression neuropathies at the elbow and wrist. Another cause of ulnar nerve palsy may be due to a failure to splint the hand in an intrinsic-plus posture following a crush injury. There are a few systemic diseases which may also lead to ulnar nerve palsy. These include leprosy, syringomyelia, and Charcot-Marie-Tooth disease. However, these systemic diseases usually involve more than one nerve.
Claw Hand can be congenital or acquired. Men are more likely to acquire the condition than a woman, but the congenital form of claw hand is distributed evenly among men and women. There are no racial or ethnic preferences for claw hand.
Pathoanatomic components relate to the imbalance between the extrinsic and intrinsic muscles. Weakened intrinsic muscles lead to a loss of MCP flexion and a loss of interphalangeal (IP) extension. Strong extrinsic muscles will lead to an unopposed extension of the MCP joints. The flexor digitorum profundus and flexor digitorum superficialis muscles not innervated by the ulnar nerve remain strong and lead to unopposed flexion of the PIP and DIP joints.
Initial presentation will include a decrease in normal hand function.
The MCP joints will be hyperextended, and the IP joints flexed.
The second and third digits will not be as involved as the fourth and fifth digits with a true ulnar nerve palsy. This is because the median nerve innervates the lumbricals involving the second and third digits, and the ulnar nerve innervates the lumbricals involving the fourth and fifth digits.
The patient may also exhibit functional weakness while attempting a grasp, grip or pinch.
A provocative test for claw hand is bringing the MCP joints into flexion. This will correct the DIP and PIP joint deformities.
Several other specific tests for ulnar nerve palsy include:
Electromyographic and nerve conduction velocity studies are used to evaluate the ulnar nerve pathology and to rule out other diagnoses.
Nonoperative management is applied if a fixed flexion contracture of more than 45 degrees occurs at the PIP joint. A strenuous hand therapy program is utilized involving serial casting.
The majority of cases will need operative management in the form of contracture release and passive tenodesis versus active tendon transfer. This treatment is reserved for those patients with a progressive deformity that is affecting their quality of life. The goal is to prevent lasting MCP joint hyperextension.
Differential diagnosis should include cervical radiculopathy and lower brachial plexopathy.
A very experienced hand therapist plays a vital role in the postoperative care of tendon transfers for ulnar nerve palsy. Protecting the transfers with custom splints while mobilizing uninvolved joints requires strict adherence to postoperative protocols. Following most procedures, the hand is immobilized for 3 to 4 weeks, followed by a blocking splint to allow motion within the restraints of the splint for the next 3 to 4 weeks. Passive exercises are started at 6 weeks and strengthening at 8 weeks for the adductorplasty and 10 to 12 weeks for the intrinsic tendon transfers.