A person after sleeping overnight with the arm under his head now experiences paresis but no numbness in the morning. Which of the following is the best explanation for it?

Correct Answer: C. A fibers are more susceptible to pressure changes than C fibers

This question tests understanding of differential nerve fiber susceptibility to mechanical compression. When an arm is slept upon, external pressure compresses the nerve trunk. The clinical presentation—paresis without numbness—is the key discriminator.

Motor function (mediated by A-alpha fibers) is lost while sensory function (mediated by C fibers for pain/temperature) is preserved. This dissociation occurs because A fibers have larger diameter and higher metabolic demands; they are exquisitely sensitive to mechanical compression and ischemia from pressure. C fibers, being unmyelinated and smaller, are more resistant to pressure-induced conduction block.

The mechanism: Pressure occludes blood supply and mechanically deforms the myelin sheath of large myelinated A fibers, causing conduction block within minutes. C fibers, lacking myelin and having lower conduction velocity, tolerate pressure better because their smaller cross-sectional area experiences less mechanical stress and their lower metabolic rate allows survival under hypoxic conditions longer.

This is pressure-induced neuropraxia, a classic Indian medical school teaching scenario. The paresis resolves within hours as pressure is relieved and A-fiber conduction recovers. This is NOT axonal damage (which would cause numbness and prolonged recovery). The answer directly states A fibers are more susceptible to pressure changes—the operative mechanism here—not hypoxia alone.

Why the other options are wrong

A. A fibers are more sensitive to hypoxia than B fibers — While A fibers are indeed more metabolically active and hypoxia-sensitive than B fibers, this option misses the primary mechanism in pressure-induced nerve compression. The question specifically involves sleeping on the arm—a mechanical pressure scenario, not pure hypoxia. Additionally, B fibers (preganglionic autonomic) are not the relevant comparison; the clinical picture involves motor (A-alpha) vs. sensory (C) dissociation. This is a distractor that focuses on hypoxia when pressure is the dominant pathophysiology. B. A fibers are more susceptible to hypoxia than C fibers — Although A fibers ARE more hypoxia-sensitive due to higher metabolic demands and reliance on oxidative phosphorylation, this option again emphasizes hypoxia over the mechanical pressure component that is central to the clinical scenario. In pressure neuropraxia, the primary insult is mechanical deformation and local ischemia from compression, not systemic hypoxia. C fibers' resistance to hypoxia is true but irrelevant to the pressure-compression mechanism. This is an NBE trap using a true statement in the wrong context. D. C fibers are more sensitive to pressure than A fibers — This is the direct opposite of the correct answer and represents a fundamental misunderstanding of fiber physiology. C fibers are actually resistant to pressure because they are unmyelinated, smaller in diameter, and have lower metabolic demands. A fibers, being large and myelinated, are highly susceptible to pressure-induced conduction block. This option reverses the pathophysiology and would predict sensory loss (C-fiber dysfunction) with preserved motor function—the opposite of what is observed clinically.

High-Yield Facts

Mnemonics

MACS Rule for Fiber Susceptibility Motor (A-alpha) = Mechanical pressure sensitive; Autonomic (B) = Anoxia sensitive; C fibers = Can tolerate pressure. In compression injuries, motor goes first (paresis), sensation spared (no numbness). BIG = VULNERABLE Big fibers (A-alpha, A-beta) are Vulnerable to Pressure because they are myelinated and metabolically demanding. Small fibers (C) are Sturdy against Pressure.

NBE Trap

NBE pairs hypoxia (options A and B) with pressure neuropraxia to trap students who conflate the two mechanisms. While A fibers ARE hypoxia-sensitive, the question's mechanical compression scenario makes pressure susceptibility the discriminating answer. Students who memorize "A fibers are hypoxia-sensitive" without understanding the context of pressure-induced neuropraxia will fall into this trap.

Clinical Pearl

In Indian clinical practice, "Saturday night palsy" (radial nerve compression from sleeping with arm over chair) and "honeymoon palsy" (ulnar nerve compression) are classic bedside examples of pressure neuropraxia. Patients present with isolated motor weakness (wrist drop, claw hand) without sensory loss—a pattern that immediately suggests A-fiber mechanical compression rather than C-fiber involvement. Recovery is complete within 2–3 weeks as the patient avoids the offending pressure.

_Reference: Guyton & Hall Textbook of Medical Physiology Ch. 45 (Nerve and Muscle Physiology); Harrison Principles of Internal Medicine Ch. 379 (Peripheral Neuropathy)_