Fixed contractures of the intrinsic muscles may severely impair the function of the hand. A mild contracture may inhibit certain hand functions without any gross deformity. The patient may complain of a weak grip when using, for example, a screwdriver or a hammer. Severe contractures cause metacarpophalangeal (MCP) joint flexion and interphalangeal (IP) joint extension, resulting in an intrinsic-plus deformity. The patient experiences difficulty in grasping, pinching, and abducting the fingers. In combination with sensory loss, the hand is severely disabled.
Individual involvement of intrinsic muscles results in characteristic deformities. Lumbrical contracture causes finger extension while the patient is trying to flex the finger. The origin of the lumbrical is pulled proximally with extrinsic flexion, and the IP joints are extended. Contraction of the abductor digiti minimi (ADM) presents as small-finger abduction and causes MCP joint flexion and IP joint extension. Thenar intrinsic muscle contracture can cause thumb adduction, MCP joint flexion, and IP joint hyperextension. The patient loses effective pinch, large-volume grip, and hand dexterity.
Intrinsic and extrinsic tightness may coexist in the same patient. Intrinsic contracture may not be clinically apparent until associated extrinsic changes are corrected. In cases of extrinsic tightness, proximal IP (PIP) joint flexion increases when the MCP joint is extended and decreases when the MCP joint is flexed. It should be kept in mind that the ability to flex PIP joints does not exclude intrinsic contracture. PIP flexion should be evaluated while the MCP joint is extended.
Intrinsic tightness or contractures should initially be treated conservatively. Such treatment includes hand therapy and splinting to increase the effective range of motion (ROM) and prevent fixed contractures. When appropriate hand therapy does not correct the disability, the following surgical options may be considered:
Hand compartment syndrome should be treated promptly.
Normal positioning and movement of the digits depends on the functional integrity of extrinsic and intrinsic muscles. The extrinsic muscles originate in the forearm, and the intrinsic muscles originate distal to the wrist. The intrinsic muscles[1] are traditionally divided into five groups (or four, if the interossei are grouped together), as follows:
The four thenar muscles are as follows:
The APB abducts the thumb away from the palm. The FPB flexes the thumb MCP joint. The opponens pollicis abducts, flexes, and pronates the first metacarpal. With these muscles, the thumb is brought from lateral to medial position across the palm in opposition to the four ulnar digits. The adductor pollicis adducts the thumb toward the palm.
The three hypothenar muscles are as follows:
The ADM abducts the little finger away from the fourth finger. The FDMB flexes the little finger at the MCP joint. The ODM abducts, flexes, and supinates the fifth metacarpal. With these muscles, the little finger is brought into opposition to the thumb.
Most anatomists describe three palmar interosseous muscles and four dorsal interosseous muscles. The dorsal interossei flex the MCP joints and extend the IP joints. The dorsal interossei also abduct the four ulnar digits from one another; the palmar interossei adduct the four ulnar digits together toward the third finger.
The four lumbrical muscles function as a connection between the flexor digitorum profundus (FDP) and the extensor mechanism. Their main function is to facilitate extension of the IP joints. The lumbricals can extend the IP joints in any position of the MCP joints.
The ulnar nerve innervates most of the intrinsic muscles in the hand: all seven interossei, the three hypothenar muscles, the adductor pollicis, the deep head of the FPB, and the two ulnar lumbricals. All of the remaining intrinsic muscles—that is, the two radial lumbricals, the APB, the opponens pollicis, and the superficial head of the FPB—are thus innervated by the median nerve.[3] (See Table 1 below.)
Table 1. Muscles of Forearm (Open Table in a new window)
Muscle |
Nerve Supply |
Muscles of anterior fascial compartment | |
Pronator teres |
Median nerve |
Flexor carpi radialis |
Median nerve |
Palmaris longus |
Median nerve |
Flexor carpi ulnaris |
Ulnar nerve |
Flexor digitorum superficialis |
Median nerve |
Flexor pollicis longus |
Anterior interosseous branch of median nerve |
Flexor digitorum profundus |
Ulnar and median nerves |
Median nerve supplies index and middle fingers in 75% of patients; ulnar nerve supplies middle, ring, and little fingers in 75% of patients (therefore, the middle finger has dual innervation in 75% of patients) |
|
Pronator quadratus |
Anterior interosseous branch of median nerve |
Muscles of lateral fascial compartment |
|
Brachioradialis |
Radial nerve |
Extensor carpi radialis longus |
Radial nerve |
Muscles of posterior fascial compartment |
|
Extensor carpi radialis brevis |
Deep branch of radial nerve |
Extensor digitorum |
Deep branch of radial nerve |
Extensor digiti minimi |
Deep branch of radial nerve |
Extensor carpi ulnaris |
Deep branch of radial nerve |
Anconeus |
Radial nerve |
Supinator |
Deep branch of radial nerve |
Abductor pollicis longus |
Deep branch of radial nerve |
Extensor pollicis brevis |
Deep branch of radial nerve |
Extensor pollicis longus |
Deep branch of radial nerve |
Extensor indicis |
Deep branch of radial nerve |
Muscles of hand lumbricals |
|
Two radial lumbricals |
Median nerve |
Two ulnar lumbricals |
Ulnar nerve |
Interossei |
Ulnar nerve |
Abductor pollicis brevis |
Median nerve |
Flexor pollicis brevis |
Median nerve |
Opponens pollicis |
Median nerve |
Adductor pollicis |
Ulnar nerve |
Abductor digiti minimi |
Ulnar nerve |
Flexor digiti minimi brevis |
Ulnar nerve |
Opponens digiti minimi |
Ulnar nerve |
Median nerve injuries are commonly referred to as high (ie, at or above the elbow) or low (ie, distal forearm to midforearm). Whereas a high injury affects both intrinsic and intrinsic motor function, a low injury affects only intrinsic motor function.
A high median nerve division paralyzes the extrinsic muscles: pronator teres, flexor carpi radialis (FCR), palmaris longus, flexor digitorum superficialis (FDS), flexor pollicis longus (FPL), radial half of the FDP, and pronator quadratus. As a result, the forearm tends to rest in supination with the wrist in ulnar deviation. The median-innervated intrinsic muscles are also paralyzed. The lumbricals to the index and long fingers are paralyzed. Therefore, only weak flexion of the MCP joints is possible with the ulnar-innervated interossei.[4, 5, 6]
The IP joints of the thumb and the index and middle fingers cannot flex as a result of paralysis of the FDP and FDS motor units. If the ulnar nerve supplies the FDP to the ring finger, the ring finger IP joints can then flex. The ulnar nerve supplies the FDP motor units to the ring and little fingers, so that the fourth and fifth fingers can flex. The APB and the opponens pollicis are paralyzed. The thumb rests in the plane of the palm and cannot be positioned for a pulp-to-pulp pinch between the thumb and fingers. The thumb IP joint is extended because of paralysis of the FPL.
Median nerve injury at the wrist preserves extrinsic muscle function. The pronator teres, FDS, FDP, and FPL motor units are intact. The first two lumbricals, the APB, and the opponens pollicis are paralyzed. When the patient slowly makes a fist, the index and middle fingers clearly lag behind the fourth and fifth fingers because of a lack of initiation of flexion at the MCP joints by the lumbricals. The thumb rests in the plane of the palm and cannot oppose the fingers (see the image below). The patient can flex the thumb terminal phalanx because the FPL is not paralyzed.
Ulnar nerve lacerations are commonly referred to as high or low to reflect whether the injury affects extrinsic and intrinsic muscles.[5, 7, 8, 9]
High ulnar nerve injury results in paralysis of the flexor carpi ulnaris (FCU) and the ulnar half of the flexor FDPs, generally FDPs III-V. The distal phalanges of the fourth and fifth fingers cannot flex. Because the FDP motor units have a common origin, some weak flexion of the fourth and fifth fingers may be possible even if the ulnar half is supplied by the ulnar nerve. An attempt to flex the wrist results in radial deviation due to paralysis of the FCU.
All seven interossei, the third and fourth lumbrical muscles, the adductor pollicis, generally one head of the FPB, and all three hypothenar muscles (FDMB, ADM, and ODM) are paralyzed. The patient cannot adduct or abduct the fingers. If the examiner places a piece of paper between the patient's fingers, he or she cannot hold it when the paper is pulled away.
The MCP joints are hyperextended, and the IP joints are flexed. These changes are more obvious at the ring and little fingers, because the first and second lumbrical muscles are not paralyzed. This condition is called a claw-hand deformity. The thumb can weakly adduct through the extensor pollicis longus (EPL). The patient can pinch and hold a paper between the thumb and index finger by strongly flexing the IP joint with the FPL. The combination of strong IP and weak MCP flexion is called the Froment sign.
Ulnar nerve injury at the wrist spares the FCU and the medial half of the FDPs. The patient can flex the wrist and all the distal IP (DIP) joints. However, all intrinsic muscles innervated by the ulnar nerve are paralyzed, and both the claw-hand deformity and the Froment sign (see the image below) are prominent.
Open or closed trauma is the most frequent cause of intrinsic hand deformities.[10, 11] Intrinsic muscle contracture can also be caused by inflammation, tumor, central nervous system (CNS) disease, joint destruction, leprosy (Hansen disease), compartment syndrome, or rheumatoid disease. Prolonged immobilization in a tight cast or splint can cause intrinsic muscle tightness.
Although sensory loss contributes to the overall impairment, it does not contribute to the deformity. Ulnar nerve compression can occur at the elbow (the cubital tunnel) or at the wrist (in the Guyon canal) and can lead to degeneration of intrinsic hand muscles.[12] Median nerve compression associated with intrinsic loss can occur with pronator syndrome or carpal tunnel syndrome. Anterior interosseous nerve compression does not result in intrinsic loss, because this nerve innervates only the extrinsic motor units.
The most common cause of intrinsic hand deformities is trauma.
One third of all patients with rheumatoid arthritis (RA) develop some degree of intrinsic contracture during the course of their disease, Hand deformities tend to progress in RA.[13]
Peripheral nerve palsy, most commonly afflicting the ulnar nerve at the elbow, occurs in 20-25% of patients with leprosy. Claw hand due to ulnar nerve paresis is therefore the most common presentation in this group of patients.
The patient may present with a history of trauma, inflammation, tumor, leprosy disease, compartment syndrome, or rheumatoid disease.
The first dorsal interosseous muscle is tested by having the patient place the ulnar side of the hand on the examination table. The radial side of the index finger is facing up. The patient is asked to raise the index finger toward the ceiling. The examiner applies resistance and observes the patient's strength. Muscle strength testing is likely to be more sensitive if the right and left sides are tested simultaneously rather than one after the other.[14]
The second, third, and fourth dorsal interosseous muscles are tested by having the patient place the palm on the examination table. The patient spreads all of the fingers against resistance (see the image below).
The palmar (volar) interosseous muscles are examined by placing a piece of paper between the digits and having the patient hold his or her fingers tightly together as the examiner tries to withdraw the paper. The test is repeated between each of the adjacent fingers.
Adhesions and contractures of the intrinsic and extrinsic extensor muscles can limit flexion of the digits. The intrinsic tightness test can be used to differentiate extrinsic pathology from intrinsic pathology.
During a test for intrinsic tightness, the examiner usually attempts to fully flex the proximal interphalangeal (PIP) joint of an examined finger while the metacarpophalangeal (MCP) joint is kept in full extension and in full flexion. In the case of intrinsic tightness, (passive) flexion of the PIP joint is more restricted when the MCP joint is in extension than when the MCP joint is in flexion (see the image below).
If the intrinsic muscles are scarred, passive MCP joint extension increases PIP joint extension and makes passive PIP joint flexion more difficult (see the images below).
The abductor pollicis brevis (APB) is tested as the patient pushes against resistance while the thumb is in the abducted position. The opponens pollicis is similarly tested with the thumb more circumducted. The adductor pollicis is evaluated as the patient pinches a piece of paper between the thumb and index finger while the examiner pulls on the paper. The flexor pollicis brevis (FPB) is assessed with the thumb MCP joint in flexion and with resistance applied volarly.
The abductor digiti minimi (ADM) is tested by having the patient place the back of the hand on the examining table while the little finger is abducted against resistance. The flexor digiti minimi brevis (FDMB) is examined by flexing the MCP joint while the finger is adducted. The interphalangeal (IP) joints must be kept in extension. To test the opponens digiti minimi (ODM), the patient performs a pulp-to-pulp pinch by moving the little finger to the thumb.
Intrinsic tightness can result in a swan-neck deformity, which is characterized by PIP joint hyperextension and distal IP (DIP) joint flexion. The tight intrinsic muscles pull the PIP joints into extension, which allows passive DIP joint flexion. Over time, the PIP joint volar plate stretches as the extensor mechanism pulls the proximal phalanx into hyperextension. As PIP joint hyperextension increases, DIP joint flexion increases.
Intrinsic contracture disturbs fine hand-muscle balance. The fingers become stiff, function deteriorates, and the hand becomes disabled.
The boutonniere deformity involves PIP joint flexion and hyperextension of DIP and MCP joints. Attenuation of the central slip with separation from the transverse retinacular ligaments causes migration of the lateral bands volar to the PIP joint rotational axis. Thus, the lateral bands act as flexors of the PIP joint. As a result, the flexor digitorum superficialis (FDS) meets less resistance and flexes the PIP joint.
Contraction of the lateral bands and oblique retinacular ligaments prevents extension of the PIP joint. The lateral bands extend the DIP joint. The MCP joint hyperextends as the sagittal band applies traction on the extensor tendon.[15, 16]
Physical examination involves evaluation of the range of motion (ROM), both active and passive, of both DIP and PIP joints. The examiner tries to passively flex the DIP joint while passively extending the PIP joint. In the presence of boutonniere deformity, both lateral bands and oblique retinacular ligaments are contracted, and the DIP joint will not flex. The examiner flexes the PIP joint, and the DIP joint can then actively and passively flex because both the lateral bands and the oblique retinacular ligaments are now relaxed.
Routine radiographs are indicated to reveal bone or joint pathology.
Magnetic resonance neurography (MRN) and ultrasonography (US) may be useful for diagnosing and evaluating peripheral nerve pathology, including trauma.[17]
Other tests that may be helpful include the following:
Intrinsic tightness or contractures should initially be treated conservatively. Surgical therapy is indicated when appropriate hand therapy does not correct the disability.[18, 19, 20] Hand compartment syndrome should be treated promptly.
Initial conservative treatment of intrinsic tightness or contractures includes hand therapy and splinting to increase the effective range of motion (ROM) and prevent fixed contractures.[21, 22, 23, 24, 25, 26]
The potential for motor recovery guides treatment for intrinsic palsy. If recovery is anticipated, the hand should be protected with a hand-based intrinsic-minus (or anticlaw) splint that prevents full metacarpophalangeal (MCP) joint extension, thus allowing extrinsic motor units to actively extend the interphalangeal (IP) joints.[27]
When appropriate hand therapy does not correct the disability, the following surgical options may be considered. Patient education is an integral and important part of preoperative preparation.
Opponensplasty aims to restore the ability to abduct the thumb volarly from the palm and oppose against the four ulnar digits. Tendon transfers used for opponensplasty are as follows[28, 29, 30, 31] : radial slip of the flexor pollicis longus (FPL), extensor digiti minimi (EDM), palmaris longus, or flexor carpi radialis (FCR) to extensor pollicis brevis (EPB), abductor digiti minimi (ADM), flexor carpi ulnaris (FCU) extended with a tendon graft, fourth-finger FDS, and extensor indicis proprius (EIP).
One of several commonly used tendon transfers employs the FDS of the fourth finger as a motor. The tendon is divided close to its distal insertion and rerouted around the FCU at the wrist. A pulley must be created to prevent proximal migration of the transferred tendon, which is passed in a subcutaneous path across the base of the hand to the MCP joint of the thumb, where it is inserted at the radial side of the thumb MCP joint. The transfer restores thumb rotation for a pulp-to-pulp pinch between the thumb and finger pads.
The thumb should be immobilized in opposition, with the wrist in neutral position, for 3 weeks with splints. After 3 weeks, all splints are removed and ROM exercises started.
This procedure is performed for loss of thumb abduction and opposition.[32] Camitz transfer provides palmar abduction rather than thumb opposition. A carpal tunnel incision is performed with a distal forearm extension. The distal palmaris longus is dissected free with a strip of palmar fascia attached. The strip of palmar fascia is tubed with sutures.
A tunnel is created in the subcutaneous tissues from the distal forearm to the radial aspect of the MCP joint of the thumb. The fascial extension of the tendon is passed through the tunnel and secured to the abductor pollicis brevis (APB) tendon. Maximal tension is required with the wrist in neutral position.
The thumb should be immobilized in opposition, with the wrist in neutral position, for 3 weeks with splints. After 3 weeks, all splints are removed and ROM exercises started.[33]
Crossed intrinsic transfer is indicated for ulnar drift in the rheumatoid hand. When necessary, it can be combined with an arthroplasty.
Interossei are released from the ulnar aspect of the second, third and fourth fingers and transferred to the radial side of the adjacent fingers to provide additional radial stability. The second web is incised, and the first palmar (volar) interosseous muscle is exposed. The first palmar interosseous tendon is divided at the middle of the proximal phalanx and dissected free from central and lateral slips. It is then sutured to the distal attachment of the radial collateral ligament of the MCP joint of the third finger.
In the same way, the procedure can be repeated in the third and fourth webs. ADM and flexor digiti minimi brevis (FDMB) tendons are divided.
A dynamic extension splint keeps MCP joints in extension and radial deviation. Active flexion exercises are initiated postoperatively.
Several classic reconstructions are described above. However, prior to any active transfer, an inventory of the active and paralyzed motor units must be made. Selection of an appropriate motor unit for transfer depends on its dispensability, length, excursion, power, and synergy with other motor units.
This procedure is indicated when intrinsic muscles are not functional. The skin is incised at the level of the MCP joints, and interossei and ADM tendons are resected. If the MCP joint is stiff, the accessory collateral ligaments or the volar plate is released. The PIP joints are then examined. PIP residual extension contracture requires lateral band tenotomy at the middle of the proximal phalanx. This can be done with a new skin incision or longitudinal extension of the first incision over the MCP joints.
MCP joints are held with Kirschner wires (K-wires) in extension for 3 weeks. PIP ROM exercises should be started immediately after the procedure.
The Littler procedure is indicated for intrinsic tightness without significant stiffness of the MCP joint. In this operation, the lateral band tenotomy is performed and the oblique fibers of the extensor hood excised. A dorsal skin incision from the MCP joint to the PIP joint provides access to the extensor mechanism. Only the oblique fibers of the extensor hood are divided. Lateral bands are divided proximal to the conjoint tendons.
MCP joints are maintained at full extension with volar splints for 2 weeks. PIP joints are not splinted, and ROM exercises are started immediately. MCP exercises are started 2 weeks later.
This procedure is indicated for PIP hyperextension caused by contractures.
Lateral bands are divided at the proximal one third of the proximal phalanx. They are then dissected free from the central slip and triangular ligaments until the distal end of the middle phalanx. The lateral bands are placed volar to Cleland's ligament, thus being rerouted volar to the axis of motion of the PIP joint. The free end of the lateral band is attached to the flexor tendon sheath at the base of the PIP joint or through a drill hole to the neck of the proximal phalanx. In this way the PIP joint is held at 30º of flexion.
A PIP dorsal extension splint is placed for 6 weeks, and flexion exercises are started immediately after the procedure.
This technique is indicated for severe swan-neck deformity. A distal intrinsic release is performed. A free tendon graft is secured on the base of the distal phalanx or the terminal extensor tendon. The graft is placed deep to the neurovascular bundle and obliquely across the volar aspect of the flexor tendon sheath proximal to the PIP joint. It is secured into the neck of the proximal phalanx with a tunnel or a pull-out suture technique holding the PIP joint in 30-40º of flexion.
An extension block splint is placed for 6 weeks, and the pull-out sutures are removed at 4 weeks. PIP joint active flexion exercises should start immediately.
The interosseous slide is indicated for interossei if muscle activity is still present. The dorsal interosseous fascia is incised, and all interossei are subperiosteally dissected free from their origins. The ADM and FDMB tendons are divided. The MCP joints are kept extended and the PIP joints flexed with a splint for 3 weeks. ROM exercises are then performed.
Lumbrical release is indicated for lumbrical muscle contracture. Contracture of the lumbrical muscles places the fingers in an intrinsic-plus position. The diagnostic test is the intrinsic tightness test. The radial lateral band with or without its oblique fibers is resected. Passive and active ROM exercises should be started immediately.
PIP joint arthrodesis with intrinsic muscle release may be indicated for advanced or complex contractures with joint fibrosis.
Excision may be indicated for fibrotic and nonfunctional adductor pollicis and first dorsal interosseous muscles. The slide procedure is indicated for functional muscles. Both muscles are released from metacarpals. Opponensplasty may be necessary as a result of the underlying condition. The first web space is maintained with K-wires placed between the first and the second metacarpals. This may create an open wound with skin deficit. The defect on the first web space is covered with a skin graft.
This procedure is designed to provide integration of MCP and PIP joint motion. The distal palmar crease is incised with a transverse incision. The FDS is divided and split into two slips. Both slips are passed volarly through the A1 or A2 pulley and sutured to themselves.[34] MCP joints are held in 20-30º of flexion and PIP joints extended with a cast for 5 weeks. Active ROM exercises are then begun.[35]
In a systematic review of various tendon transfers for operative management of ulnar nerve paralysis, Schaeffer et al determined that the evidence supported FDS lasso transfer if the primary goal was improvement in the appearance of claw deformity, but that the evidence favored ECRL four-tail transfer if the primary concern was grip strength; adductorplasty alone was found to be most effective when pinch strength was functionally limiting.[36]
Fowler used the EDM and the EIP for direct transfers to the lateral bands of the extensor mechanism. Intrinsic-plus deformity was common because of excessive tension. In patients in whom the EDM was the only effective little-finger extensor, little finger extension was lost.
Casts, splints, and dressings should not be tight. The thumb should never be splinted in adduction. Dependent edema can be avoided by raising the hand. Prompt treatment of compartment syndrome with surgical release of all interspaces is done when indicated. Immediate initiation of ROM exercises, when indicated, is a requirement for the best functional outcome.
For optimal postoperative results, patients should follow hand-therapy protocols.