A 45-year-old man presents with progressive weakness of grip and a characteristic hand deformity. Clinical examination reveals hyperextension at the metacarpophalangeal joints with flexion at the interphalangeal joints of the 4th and 5th fingers bilaterally. Sensory loss is noted over the medial 1.5 fingers. The structures marked **C** in the diagram are responsible for the loss of motor function. Which of the following best explains the mechanism of the observed deformity?

Explanation

## Why "Loss of interossei function → unopposed action of extensor digitorum at MCP joints and FDP at IP joints → claw hand" is right The interossei (marked **C**) are innervated entirely by the ulnar nerve (deep motor branch). These muscles perform two critical functions: the dorsal interossei abduct the fingers (DAB), and the palmar interossei adduct them (PAD). More importantly, the interossei act as MCP flexors and IP extensors via their insertion into the extensor apparatus (lateral bands). When the ulnar nerve is injured (commonly at the elbow in cubital tunnel syndrome or medial epicondyle fractures, or distally at Guyon's canal), all interossei are paralyzed. This results in unopposed action of the extensor digitorum (which extends MCP joints) and the flexor digitorum profundus (which flexes IP joints), producing the characteristic "claw hand" or "ulnar claw" deformity with MCP hyperextension and IP flexion, particularly prominent in the 4th and 5th fingers. The sensory loss over the medial 1.5 fingers (little finger and medial half of ring finger) confirms ulnar nerve injury. (Gray's Anatomy 42e, Ch 49) ## Why each distractor is wrong - **Loss of lumbricals → unopposed action of flexor digitorum superficialis at PIP joints → swan neck deformity**: Lumbricals (marked **D**) are innervated by both median (1st–2nd) and ulnar (3rd–4th) nerves. While lumbrical paralysis contributes to claw deformity, lumbricals are not the sole cause of the observed pattern. Swan neck deformity (PIP hyperextension with DIP flexion) is characteristic of rheumatoid arthritis or intrinsic muscle tightness, not isolated lumbrical loss. The clinical presentation here is classic claw hand, not swan neck. - **Loss of thenar muscles → thumb adduction weakness with compensatory IP flexion → Froment sign positive**: Thenar muscles (marked **A**) are innervated by the median nerve (recurrent branch), not the ulnar nerve. While Froment sign (positive thumb IP flexion during paper grip test due to adductor pollicis weakness) is indeed a sign of ulnar nerve injury, it does not explain the claw deformity of the 4th and 5th fingers. The question specifically asks about the hand deformity pattern observed, which is claw hand, not thumb weakness alone. - **Loss of flexor digitorum profundus → loss of DIP flexion with preserved MCP extension → intrinsic plus position**: FDP is innervated by the ulnar nerve (medial half) and anterior interosseous nerve (lateral half), not by the interossei. Loss of FDP would result in inability to flex the DIP joints, producing a "lumbrical plus" or intrinsic plus appearance (MCP flexion with IP extension), which is the opposite of claw hand. The clinical picture here is claw hand (MCP extension, IP flexion), not intrinsic plus. **High-Yield:** Ulnar nerve injury → all interossei paralyzed → claw hand (MCP hyperextension + IP flexion in 4th–5th fingers); worse with proximal lesions if FDP is spared ("ulnar paradox"). [cite: Gray's Anatomy 42e, Ch 49]