A patient presented with the extension of MCP joint and flexion of IP joints. Which muscle is affected?

Correct Answer: A. Interossei and lumbricals

The clinical presentation of MCP extension with IP flexion is the pathognomonic sign of intrinsic hand muscle paralysis, specifically loss of interossei and lumbricals function. These muscles have dual actions: (1) MCP flexion via their flexor action at the MCP joint through insertion into the volar plate and flexor hood, and (2) IP extension via their extensor action on the IP joints through the extensor expansion (dorsal hood). When these intrinsic muscles are paralyzed (as in ulnar nerve injury affecting interossei, or combined ulnar + median nerve injury affecting lumbricals), the unopposed action of the extrinsic extensors (extensor digitorum, extensor carpi radialis) causes MCP extension, while the extrinsic flexors (flexor digitorum superficialis and profundus) cause IP flexion. This creates the characteristic "claw hand" deformity. The lumbricals (innervated by median nerve to digits 1–2, ulnar nerve to digits 3–4) and interossei (all ulnar nerve) are the only muscles capable of simultaneously flexing MCPs and extending IPs—a unique biomechanical property that makes this sign diagnostic for intrinsic paralysis. This is a high-yield anatomy-clinical correlation tested frequently in NEET PG.

Why the other options are wrong

B. Abductor pollicis longus — This muscle abducts the thumb at the CMC joint and extends it at the MCP joint; it has no action on IP joints. Paralysis would cause thumb adduction and loss of thumb abduction, not the MCP extension + IP flexion pattern described. This is a distractor targeting students who confuse thumb anatomy with finger intrinsic function. C. Extensor digitorum — Extensor digitorum extends both MCP and IP joints (via the extensor expansion). Paralysis would cause loss of extension at both joints, producing the opposite clinical sign (flexion at both MCP and IP). This is an NBE trap: students may incorrectly assume that any extensor paralysis causes the described deformity, when in fact loss of intrinsic muscles unmasks extrinsic extensor action. D. Abductor pollicis brevis — This thenar muscle abducts the thumb at the MCP joint and is innervated by the median nerve (recurrent branch). Its paralysis causes loss of thumb abduction and opposition, not the finger claw deformity. This is a distractor for students confusing thumb-specific intrinsic muscles with the lumbricals and interossei that control finger posture.

High-Yield Facts

Mnemonics

CLAW = Intrinsic Loss Claw hand = Lumbricals + interossei Affected → Wrist extensors unopposed. When intrinsics are paralyzed, extrinsic extensors dominate MCPs (extend them) while extrinsic flexors dominate IPs (flex them). MCP Flex, IP Extend = Intrinsic Job Only intrinsic muscles (lumbricals + interossei) can flex MCPs while extending IPs—this is their unique dual action. Any other muscle combination produces different joint movements.

NBE Trap

NBE pairs "claw hand" with extrinsic muscle paralysis (extensor digitorum) to trap students who confuse the direction of joint movement. The key discriminator is that intrinsic paralysis unmasks extrinsic action, not that extrinsic muscles directly cause the deformity.

Clinical Pearl

In Indian clinical practice, ulnar nerve compression at the wrist (Guyon's canal syndrome) or leprosy-induced ulnar nerve damage (common in endemic regions) presents with claw hand in digits 4–5. Recognition of this sign allows rapid bedside diagnosis and guides urgent nerve decompression or rehabilitation therapy.

_Reference: Bailey & Love Ch. 56 (Hand Anatomy); Robbins Ch. 27 (Peripheral Nerve Injuries)_