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Swan-neck deformity

A swan-neck deformity, defined as proximal interphalangeal (PIP) joint hyperextension with concurrent distal interphalangeal (DIP) joint flexion, occurs in approximately 50% of patients with rheumatoid arthritis RA. However, swan-neck deformity is not unique to RA, because it may also be congenital or traumatic in nature.

It may also caused by:
# mallet finger (due to rupture of lateral slips at their junction with bone)
# cerebral palsy (due to muscle imbalance)
# congenital joint laxity

The pathophysiology of the swan-neck deformity begins with flexor synovitis, which increases the flexor pull on the MP joint. Constant efforts to extend the finger against this pull lead to stretching of the collateral ligaments and the volar plate at the PIP joint.

In a normal finger, intrinsic muscles (interosseous and lumbrical) insert into the lateral bands and serve as flexors of the MP joint and extensors of the PIP and DIP joints by being located volar to the MP joint axis and dorsal to the PIP and DIP joint axes.

In a rheumatoid finger, the lateral bands are constrained in their dorsal position, upsetting the flexor-extensor balance. In this position, the lateral bands increase the pull of the long extensor tendon's central slip, which attaches to the dorsal base of the middle phalanx. The increase of flexor profundus tension resulting from hyperextension of the PIP joint leads to a reciprocal flexion of the DIP joint. Progressive disease causes joint destruction and fixed contracture.

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