INTRINSIC MUSCLE CONTRACTURES

The mid-axis of the hand, as viewed from the dorsum, is
defined as the central axis of the third metacarpal. The dorsal
interosseous muscles abduct the fingers from this axis, whereas the
palmar interosseous muscles adduct them. There are four dorsal and
three palmar interosseous muscles. In addition, there are three
hypothenar muscles

that
function like dorsal interosseous muscles. Dorsal interosseous muscles
arise from the metacarpal shafts and insert so as to achieve digital
abduction; the designation of first dorsal interosseous muscle thus
belongs to that muscle on the radial side of the index finger, and so
on, in an ulnar direction. The little finger is actually abducted by
the abductor digiti quinti; the middle finger is abducted in both a
radial and an ulnar direction and, therefore, has two dorsal
interosseous muscles (2,3,6,15,20).

Except for the third, the dorsal interosseous muscles
have two muscle bellies and therefore two (tendon) insertions—one into
the base of the proximal phalanx and the other via the dorsal (tendon)
mechanism (Fig. 63.1). The bony insertion
deviates the digit and has a mild effect on proximal phalangeal
[metacarpophalangeal (MP) joint] flexion. The tendon insertion produces
MP joint flexion via the transverse fibers over the dorsum of the
proximal phalanx. The tendon insertion also assists with proximal
interphalangeal (PIP) and distal interphalangeal (DIP) extension via
the oblique fibers that continue distally to join the lateral slips of
the extensor tendon, forming the conjoined lateral band. The (radial
and ulnar) lateral bands unite over the dorsum of the middle phalanx to
become the terminal tendon. The abductor digiti quinti inserts into
bone on the ulnar side of the proximal phalanx of the little finger,
and the flexor digiti quinti brevis forms the ulnar lateral band in the
little finger. The palmar interosseous muscles also arise from the
metacarpal shafts, but each has only one muscle belly. None has a bone
insertion into the proximal phalanx, but each functions as do the
lateral bands from the dorsal interossei (via the transverse fibers,
conjoined lateral band, and terminal tendon). The opponens digiti
quinti, the most dorsal of the three hypothenar muscles, has an unusual
insertion into the ulnopalmar shaft of the fifth metacarpal, producing
carpometacarpal flexion and supination when it contracts.

The lumbricals extend the PIP and DIP joints but also
assist in flexing the MP joints. The lumbricals are unique in that they
arise on their antagonist, originating from the tendons of the flexor
digitorum profundus in the mid palm (Fig. 63.2).
Lumbricals of the index and middle fingers originate from the radial
side of the respective flexor digitorum profundus tendons. Lumbricals
of the ring and little fingers originate from bipennate muscle bellies
on the adjacent surfaces of the flexor digitorum profundus tendons.
Lumbrical tendons course distally palmar to the deep transverse
intermetacarpal ligaments, becoming part of the radial lateral bands at
the midportion of the proximal phalanges. When the lumbrical muscles
contract, they pull the flexor digitorum profundus tendon distally,
decreasing its flexion effect (relaxing the antagonist), as well as
pulling proximally on the lateral band and terminal tendon, thereby
extending the PIP and DIP joints.

The extrinsic extensor tendons are the only extensors of
the proximal phalanges (MP joints), lying in the dorsal midline and
inserting via the sagittal bands (Fig. 63.3).
These aponeuroses pass in a palmar direction, attaching into the palmar
plate and base of the proximal phalanges. The sagittal bands (extrinsic
extensor fibers) are proximal and medial to the transverse fibers
(intrinsic flexor fibers). It is important not to confuse the sagittal
bands with the transverse fibers, since the sagittal bands arise from
the extensor tendon, pass in a palmar direction, and extend the finger,
whereas the more distal transverse fibers arise from the lateral band
and pass dorsally, insert into the dorsal tendon mechanism (not bone),
and flex the proximal phalanx (Fig. 63.4) (9,18,20,31,36).

Intrinsic muscles flex the MP joints, extend the
interphalangeal joints, and deviate the fingers. Therefore, intrinsic
contractures, with concomitant loss of compliance or elasticity, would
be expected to interfere with interphalangeal joint flexion and MP
joint extension. Less severe contractures tend to affect the
interphalangeal joints, whereas more severe contractures produce
deformity at both levels.

Intrinsic muscle tightness, or an intrinsic contracture, should be suspected when active PIP flexion is limited (Fig. 63.5).
A simple physical test will usually confirm the diagnosis. Passive PIP
flexion is tested by the examiner while the MP joint is held flexed; it
is then tested again while the MP joint is held extended. A test of
intrinsic tightness is positive if there is significantly less passive
PIP flexion with the MP joint extended than with it flexed. Many
authors have described this test, and it is often (confusingly)
recorded eponymically (7,10,30,34).
In contrast, extrinsic tightness (contracture of the extensor tendons)
is present if passive PIP flexion is more limited when the MP joint is
flexed than when it is held in extension. It may be impossible to
perform these tests effectively if there are contractures in the MP or
PIP joints, or if a joint is dislocated. If there are both intrinsic
and extrinsic contractures simultaneously, one may obscure the other.

The most common presentation of a functionally
significant intrinsic contracture follows trauma, probably caused by
muscle changes as a consequence of edema, anoxia, and immobilization.
For example, a patient may complain that she cannot grasp objects;
sometimes patients report weakness. A careful history and examination
will reveal the intrinsic muscle pathology. When examined in the
office, the patient may be almost able or fully able to make a fist
with unrestricted simultaneous MP and PIP flexion. In attempting to
grasp a hammer, however, the flexion of the MP joints is blocked by the
hammer, and active flexion of the PIP joints is decreased. This
activity is a functional test of intrinsic tightness.

After trauma, the moderately edematous hand is likely to
develop intrinsic tightness that affects the PIP joints exclusively.
When the hand is unprotected and swollen, MP joint flexion also becomes
difficult. The intrinsic muscles, however, can achieve relatively
unresisted PIP extension because the capsule and collateral ligaments
are initially more lax in that position. Continued PIP extension via
tight intrinsic muscles results in limited PIP flexion; in severe
cases, it may also be associated with actual capsular tightness at the
PIP level. The intrinsic tightness test is positive in such cases.

An extended anoxic injury, severe swelling, and
prolonged elevated compartment pressure will produce intrinsic
myonecrosis with secondary fibrosis, causing deformities at both the MP
and the interphalangeal joints (2,3,18,19,34,36).
These MP flexion contractures result only from marked and severe
intrinsic fibrosis, as evidenced by the fact that most significant
posttraumatic MP joint deformities are extension contractures resulting
from tight collateral ligaments and secondary capsular scarring. The
swollen MP joints strongly resist being flexed, and only in the
presence of marked intrinsic muscle scarring will a contracture be
severe enough to force the already tight, extended MP joints into a
flexed position. Severe PIP extension or hyperextension may also be a
part of this often static deformity. Secondary changes at both joints,
with pericapsular fibrosis in the deformed position, are not uncommon.
Often the first web is also limited because of contracture of the
adductor pollicis and the first dorsal interosseous muscles. A
significant degree of hand dysfunction results from these contractures.

Intrinsic spasticity may cause dysfunctional deformities
in patients with cerebral palsy; it may also occur following
cerebrovascular accidents, and it may also affect patients with central
nervous system diseases (11,19,24,26,27,33).
At times, the intrinsic spasticity is not clinically evident until
after the tighter and stronger finger and wrist flexors have been
released surgically. Weeks or months after a flexor release or slide,
the previously corrected digits may begin to assume an intrinsic-plus
posture, with combined MP flexion and PIP extension or hyperextension,
often appearing unexpectedly. Although this deformity is similar to
that associated with severe posttraumatic contracture, the cause and
treatment are different. This condition is attributable to overactive
muscles, not scarred and necrotic tissue. The purpose of a surgical
release is ideally to decrease the spasticity, and to lengthen the
intrinsic muscle–tendon unit to correct the deformity and preserve
function. Strictly speaking, the intrinsic muscle cannot be lengthened;
however, such an effect is attainable via a muscle slide (31,32).

When the terminal extensor tendon is divided or avulsed,
the proximal part of the terminal tendon and contiguous conjoined
lateral bands retract proximally, unbalancing the extensor forces at
the PIP joint. A hyperextension deformity of the PIP joint may
gradually develop, or the joint may merely become more difficult to
flex actively (14,27). The intrinsic tightness test is typically positive.

Repair of the terminal tendon as well as intrinsic
stretching exercises may be required to correct this problem. Digital
rebalancing may have to be undertaken in resistant cases. The need for
tendon transfer release or capsulodesis is determined by a careful
assessment of the combined effects of the intrinsic and extrinsic
tendon contributions to the PIP overpull.

The lumbrical is a unique muscle that both arises from
and inserts into a tendon, relaxing its antagonist when functioning.
Normal PIP flexion depends on balanced flexor digitorum profundus
contraction and lumbrical relaxation. Lumbrical scarring (shortening)
and loss of elasticity cause transmission of flexor digitorum profundus
traction into the lumbrical tendon, to which it has become tethered,
rather than through the more distal portion of the flexor digitorum
profundus tendon (Fig. 63.10A). Active pull on the flexor digitorum profundus tendon then causes PIP and DIP extension via the contracted lumbrical,

rather than flexion, a situation Parkes termed the “paradoxical lumbrical-plus finger” (25).

Paradoxical lumbrical transmission of flexor forces may
also be seen when the normal flexor digitorum profundus insertion is
lost, as may occur in untreated distal tendon lacerations or distal
joint amputations (Fig. 63.10B). The then-lax
profundus tendon retracts proximally, and contraction of the flexor
digitorum profundus muscle is transmitted to the dorsum of the PIP
joint via the lumbrical tendon, producing paradoxical extension or
limited active flexion. A loosely inserted tendon graft would have the
same effect. The intrinsic tightness test is positive in such cases.

Resection of the radial lateral band will cure this
problem. Indeed, I am careful to test patients with DIP amputations for
intrinsic tightness, and I often perform an acute radial lateral band
release. Intrinsic stretching exercises become a regular part of the
rehabilitation program.

Interosseous contracture is common in the patient with
rheumatoid arthritis. Unlike posttraumatic deformities, contracture may
be associated with painful synovitis, ulnar digital drift, joint
subluxation, and joint destruction. Secondary deformities are common
and may require a combination of joint and tendon reconstruction and
releases (5,8,35,37).
It is beyond the scope of this chapter to discuss correction of
rheumatoid ulnar drift, intrinsic tenodesis, and spiral oblique
retinacular ligament reconstruction (see Chapter 70).

The most common problem accompanying intrinsic tightness
and contractures is failure to recognize the underlying cause of
limited PIP motion following injury. Intrinsic contractures are far
more common than generally appreciated. Adequate correction requires
accurate diagnosis. When active PIP flexion is limited as a result of
posttraumatic hand edema, suspect intrinsic tightness and impending
contractures and perform an intrinsic tightness test. Prompt
institution of intrinsic muscle-stretching exercises and regular
supervised therapy will often prevent the development of deformity and
fixed contractures.

Surgical release of the intrinsic muscles, when
required, should not be considered an end in itself, but rather a means
to an end—a second chance at therapy. Intrinsic contracture destroys
the delicate balance of the hand. Intrinsic release will not achieve
functional improvement unless these very demanding and unforgiving
small joints and tendons are made to glide in order to regain the full
range of motion in the postoperative interval. Select patients
carefully, and make every effort to help them understand the crucial
role they will play in their own recovery. Patients who are not
intellectually and emotionally committed to a recovery that requires
tediously repetitive therapeutic exercises, including frequent hand
therapy and office visits, should not undergo the procedure.

The author wishes to acknowledge John A. Nyquist for the
illustrations in this chapter, and Frances S. Sherwin for editorial
assistance.