The initial event in the evolution of the development of a Boutonnière deformity is:
Loss of continuity of the central slip insertion into the back of the base of the middle phalanx. The initial event in the development of a Boutonnière deformity is loss of continuity of the central slip insertion into the back of the middle phalanx base. This is followed by dissociation of the central slip from the lateral bands and palmar migration of the lateral slips until they go past the axis of the joint and become flexors. The back of the joint ‘buttonholes’ through the extensor mechanism. This position rapidly becomes fixed. The lateral slips now act entirely on the DIP joint producing hyperextension. Rigid flexion contracture of the PIP joint is a secondary, non-specific outcome of prolonged flexion of this joint.
In the correction of a swan neck deformity by operative procedure, it is essential to:
Achieve slight flexion or a neutral position of the PIP joint. The determining event in development of a swan neck deformity is hyperextension at the level of the PIP joint. This can be secondary to an uncorrected mallet deformity (when the long extensors, unable to extend the DIP joint, overextend the PIP joint), malunion in extension of a fracture around the PIP joint, or loss of flexing forces at the PIP joint, the volar plate and the FDS being the main factors. All conservative or operative methods of swan neck correction include, as an essential feature, correction of the PIP joint to neutral or slight flexion.
Of the lumbrical muscle, all statements are true except:
It is an abductor of the digit. This statement is incorrect; the lumbrical has no attachment to bone. It arises from the tendon of FDP and inserts into the long extensor complex. The lumbrical flexes the MCP joint and extends the PIP joint. Paralysis results in the opposite of such actions, the claw posture (or ‘intrinsic minus position’), which consists of a hyperextended MCP joint and a flexed PIP joint. The lumbrical has no radial deviation vector on the digit.
Bilateral radial dysplasia with present thumbs of relative normal size is seen in association with:
TAR syndrome. Thrombocytopenia-absent radius (TAR) syndrome is an autosomal recessive disorder characterised by congenital thrombocytopenia, leukocytosis and bilateral total aplasia of the radius with present thumbs. Although the thumb in TAR syndrome patients is of relatively normal size and shape, it is held in a position of MCP flexion in most patients and function is impaired.
References: 1. Goldfarb CA, Wustrack R, Pratt JA, Mender A, Manske PR. Thumb function and appearance in thrombocytopenia-absent radius syndrome. J Hand Surg [Am] 2007; 32(2): 157-61.
In the proximal row of the carpus, radiological signs of a ruptured scapholunate ligament include all but:
An extended scaphoid. A wide gap between scaphoid and lunate is otherwise known as the Terry Thomas sign in reference to a British actor with a gap in his teeth. A flexed scaphoid leads to the signet ring sign on plain radiography. The radiological gap between scaphoid and lunate should be equal to that of other intercarpal joint spaces. The kinetics of the carpus produces a strong tendency for the scaphoid to flex and the triquetral to extend, with the lunate linking these two conflicting forces. Dissociaton between the scaphoid and lunate permits the scaphoid to flex, while the lunate, under the pull of the triquetrum, via the luno-triquetral ligament, extends (dorsal intercalated segment instability [DISI]).
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