A common clinical deformity is ‘claw hand’, also known as the ‘intrinsic minus’ hand. This is characterised by hyperextension of the metacarpophalangeal joints and flexion of the proximal and distal interphalangeal joints. Any functional deformity of this type results from an imbalance of the actions of the tendons acting in this region. The intrinsic tendons of the fingers, namely lumbricals and interossei, span the metacarpophalangeal joints palmar to their axis of rotation and function to flex these joints. The lumbricals act more powerfully than the interossei because they attach more distally and have a greater moment of force. Beyond the metacarpophalangeal joints these tendons continue on as the lateral bands of the extensor tendons linking with the extensor mechanism and pass dorsal to the axis of the proximal and distal interphalangeal joints thus extending these joints. The interosseous muscles also insert into the bases of the proximal phalanges, such that the dorsal interossei abduct the fingers from each other while the palmar interossei adduct. Loss of function of intrinsics leads to an imbalance of the tensions between the long extrinsic (extensor and flexors) and the short intrinsic muscles. The resting tone of the intrinsics is lost leading to unopposed long extensors across the metacarpophalangeal joints and unopposed long flexors across the interphalangeal joints, resulting in this characteristic deformity of the hand.
Ulnar nerve palsy
In this condition all interossei are paralysed as well as the ulnar-sided lumbricals, but the median nerve innervated lumbricals to the index and middle fingers are preserved. As a consequence the clawing is confined to the ring and little fingers and the thumb. The most common cause of ulnar nerve palsy is wrist laceration. At this level the proximally innervated long flexors to the ring and little fingers are intact, compared to high ulnar nerve injuries where the long flexors are also paralysed, making finger flexion and the claw deformity less obvious. Ulnar nerve compression at the elbow will cause ulnar claw and ulnar sensory loss. Spontaneous ulnar clawing with no sensory loss is most likely due to compression of the motor branch by a ganglion in the region of the piso-hamate joint.
Paralysis of the ulna and median nerves
This produces a full claw hand. This deformity will also result from C8 and T1 nerve root lesions.
Nerve palsy due to leprosy
On a worldwide basis, leprosy still remains the most common cause of the claw hand.
Certain conditions mimic the claw hand.
This deep flexor compartment compression syndrome results in ischaemic necrosis of the profundus tendons in the forearm causing flexion contracture of the fingers. The superficialis tendons are usually spared, but the intrinsic tendons may also be contracted. This produces flexion of all joints of the fingers, rather than hyperextension of the metacarpophalangeal joints. The flexor tendons are tight.
Intrinsic muscle contracture
This can be of ischaemic origin, due to crush injuries and produces the opposite deformity to the claw hand, namely tight intrinsics, or intrinsic plus hand, rather than the loose intrinsic minus claw hand. The metacarpophalangeal joints are flexed and the interphalangeal joints extended. This condition spontaneously occurs in rheumatoid arthritis and may lead to Swan neck deformity. The Bunnell test for intrinsic tightness involves passive extension of the metacarpophalangeal joint followed by assessment of the passive flexibility of the interphalangeal joints. In the normal hand when the metacarpophalangeal joint is maximally extended the interphalangeal joints can be fully flexed passively. When the intrinsics are tight and the metacarpophalangeal joints are stretched into extension, thereby further tightening the intrinsics, there will be secondary tightening of the extensor mechanism distally in the fingers, which will limit passive flexion of the interphalangeal joints. By individually manipulating the fingers into either ulnar or radial angulation and applying the Bunnell test, tightness of the radial or ulnar intrinsics can be selectively examined.
This typically involves the little and ring fingers and can mimic a claw hand, but the metacarpophalangeal joint is flexed and the contracted fingers cannot passively be extended. Palpation of the Dupuytren's tissue in the palm confirms the diagnosis.
Congenital flexion contracture (camptodactyly)
This condition usually involves only the little finger, it is often bilateral and is hereditary. It is present at birth. The finger is flexed at the proximal interphalangeal joint and often cannot be passively fully straightened.
This results from an upper motor neuron palsy and usually involves a clasping deformity of the thumb in the palm and tightening of the flexor tendons that cannot be easily passively extended. The wrist is also characteristically flexed.
Various muscular dystrophies present as bizarre hand deformities of an atypical type.
The classic claw hand involves hyperextension of the metacarpophalangeal joints and flexion of the interphalangeal joints. The ulnar nerve paralysis results in ulnar claw, where the clawing is confined to the little and ring fingers. The high ulnar palsy has less obvious clawing than the low ulnar palsy.
There is loss of abduction/adduction of the fingers and wasting of the interosseous muscles, most obvious in the first web space and the hypothenar eminence.
There will be numbness in the distribution of the involved nerve or nerves.
Frequently in ulnar paralysis, the little finger remains permanently abducted from the ring finger (Wartenberg's sign). The basis of this deformity is unclear, but in some way relates to an imbalance between the intrinsic muscles either side of the little finger metacarpophalangeal joint and the long extensor mechanism.
Median nerve thenar muscle paralysis results in the ‘simian palm’ deformity where the thumb metacarpal moves dorsally into the plane of the finger metacarpals due to the unopposed extension of the pollicis longus tendon. Abduction and opposition of the thumb are now impossible. Although the claw hand is most obviously a deformity of the fingers, the thumb is inextricably involved and disturbance of thumb function is frequently the major disability.
Weakness, especially in turning doorknobs, keys in locks and taking tops off jars is a common complaint due to the lack of abduction/adduction of the fingers. Pickup is clumsy especially in the full claw hand where the pulps of the fingers cannot be presented to the object because of inability to fully extend the interphalangeal joints. This results in the nails pushing the object away during attempts at pick-up. Thumb pinch grip is also greatly weakened and clumsy due to adductor paralysis and the collapsing interphalangeal joint converting the pulp pinch of the thumb into nail pinch. Thumb disability is further magnified in the full claw hand where median innervated thenar muscles are also paralysed. Strong power grip of the fingers into the palm, however, is retained, except where the long flexors are involved in high nerve injuries. Fixed flexion contractures of the proximal interphalangeal joints of the clawed fingers can develop as a secondary phenomenon due to lack of active extension and trophic changes may occur due to numbness. Wartenberg's abducted little finger is a frequent source of nuisance.
Nerve repair or decompression where possible is the treatment of choice. If the nerves are unrepairable or repairs have failed, tendon transfers can be considered. Tendon transfers at best correct the claw deformity and thumb collapse, but do little to restore the functional disability of loss of abduction/adduction of the fingers or thumb collapse. Various techniques have been described. Most have been designed for the management of the sequelae of leprosy.If surgical treatment cannot be offered, rehabilitation with physiotherapy and splintage may help the patient.