A 41-year-old man presents with abrupt onset of continuous severe rotatory vertigo and vomiting for 36 hours following an upper respiratory infection. Examination reveals unidirectional horizontal-torsional nystagmus with fast phase to the left, and the head impulse test shows a corrective saccade when the head is turned rapidly to the right. Pure-tone audiometry is completely normal with symmetric thresholds and preserved speech discrimination. The clinical findings marked **A** in the diagram (normal audiogram with abnormal head impulse and unidirectional nystagmus) are most consistent with vestibular neuritis. Which of the following management principles is MOST critical in the acute phase to prevent impairment of central vestibular compensation?

Why short-term vestibular suppressants (24–72 hours) followed by early mobilization is right

The clinical presentation—normal hearing, abnormal head impulse test, unidirectional nystagmus, and absence of brainstem signs—confirms peripheral vestibular neuritis (typically HSV-1 reactivation in Scarpa's ganglion). The anchor finding marked A (normal audiogram with abnormal head impulse and unidirectional nystagmus) is the diagnostic hallmark distinguishing vestibular neuritis from labyrinthitis (which includes SNHL) and central causes. Management requires a two-phase approach: (1) SHORT-TERM vestibular suppressants (promethazine, benzodiazepines, metoclopramide) for only 24–72 hours to control intractable nausea and vertigo, and (2) EARLY MOBILIZATION and vestibular rehabilitation exercises (Cawthorne-Cooksey) to accelerate central compensation. Prolonged suppressant use impairs the brain's ability to recalibrate vestibular signals, delaying recovery (Dhingra ENT 7e; Strupp NEJM 2004).

Why each distractor is wrong

Dhingra ENT 7e Ch 20; Strupp Vestibular neuritis NEJM 2004