Nystagmus: Peripheral/Vestibular Localization

Overview

Acute vestibular syndrome presents as sudden, sustained vertigo with nausea and gait instability, and it has two broad causes: a peripheral vestibular process (the inner ear or vestibular nerve) or a central one (a posterior circulation stroke affecting the brainstem or cerebellum). The distinction matters at the bedside because the two carry very different stakes. Peripheral causes are almost always benign and self-limited. Central causes can be a life-threatening stroke, and early MRI, including diffusion-weighted imaging, can be falsely negative for a small posterior fossa infarct within the first 24 to 48 hours. A well-performed bedside exam is, in that window, more sensitive than imaging.

This page covers the exam findings and waveform characteristics that point toward a peripheral cause. For the mirror-image findings, downbeat nystagmus, periodic alternating nystagmus, see-saw nystagmus, and purely torsional or vertical waveforms, see the companion page on central nystagmus.

Features of Peripheral Nystagmus

Peripheral vestibular nystagmus has a recognizable signature that differs from central nystagmus on several independent axes. No single feature is diagnostic on its own; it's the pattern taken together that makes bedside localization reliable:

• Direction: unidirectional, with the fast phase beating away from the affected ear. This reflects a tonic imbalance in vestibular signal between the two labyrinths rather than a central gaze-holding failure, and the fast-phase direction stays fixed regardless of gaze position. Central gaze-evoked nystagmus, in contrast, typically reverses direction with gaze.
• Fixation suppression: visual fixation meaningfully suppresses peripheral nystagmus, since fixation can partly override the vestibular tone imbalance driving it. Central nystagmus persists, or even worsens, with fixation.
• Alexander's law: amplitude increases when the eyes are directed toward the fast phase and decreases toward the slow phase. This pattern holds consistently in peripheral disease and much less reliably in central causes.
• Associated symptoms: cochlear symptoms (tinnitus, hearing loss) alongside intense vertigo point toward a peripheral labyrinthine or vestibular nerve cause. Brainstem or cerebellar signs such as dysarthria and limb ataxia point toward a central cause instead.

Positional nystagmus, provoked by maneuvers like Dix-Hallpike, has two further features that favor a peripheral cause, most classically benign paroxysmal positional vertigo (BPPV). The first is latency: a brief delay of several seconds before onset, the time needed for otoconial debris to shift within the semicircular canal. The second is fatigability: the nystagmus diminishes or disappears with repeated provocative testing. Central positional nystagmus begins immediately, with no latency, and does not fatigue on repeat testing.

The HINTS Exam

HINTS (Head impulse, Nystagmus, Test of Skew) is a three-part bedside battery for the patient with acute, continuous vestibular syndrome. It doesn't apply to episodic or positional vertigo.

• Head impulse test: the examiner rapidly rotates the patient's head a small amplitude while the patient fixates on a target. A normal vestibulo-ocular reflex keeps the eyes locked on target; an abnormal test shows a corrective, catch-up saccade back to the target after the head stops, indicating a deficient VOR, typically from a peripheral vestibular lesion. Counterintuitively, a normal head impulse test in an acutely dizzy patient is the finding that should worry you: it suggests the VOR arc is intact and the vertigo may instead be central.
• Nystagmus: direction-fixed, unidirectional, fixation-suppressible nystagmus favors peripheral disease; direction-changing or purely vertical or torsional nystagmus favors central disease.
• Test of skew: alternate cover testing for a vertical misalignment (skew deviation). Its presence reflects disruption of central otolithic pathways and is itself one of the three findings favoring a central, often stroke, etiology.

The mnemonic for the stroke-favoring pattern is "INFARCT": a Normal head impulse, direction-changing (Fast-phase alternating) nystagmus, or the presence of skew (Refixation on Cover Test). Any one of these three findings on its own raises concern for a central cause. The opposite pattern, an abnormal head impulse, unidirectional nystagmus, and no skew, favors a benign peripheral cause.

Bedside Examination Technique

Frenzel goggles, high-plus lenses with internal illumination, are used at the bedside to eliminate the patient's ability to visually fixate. Since fixation suppresses peripheral nystagmus, examining without blocking fixation can make a true peripheral nystagmus falsely appear absent or much subtler than it actually is. Frenzel goggles unmask it. Optokinetic nystagmus testing, using a rotating striped drum or tape, serves a different purpose: it is an involuntary reflex that cannot be voluntarily suppressed, so its presence confirms some level of functioning vision. That makes it useful when functional (nonorganic) visual loss is suspected, not for localizing vestibular disease.

Common Causes

Vestibular neuritis, an inflammatory, presumed post-viral disorder of the vestibular nerve, is the classic cause of acute peripheral vestibular syndrome. It presents with the unidirectional, fixation-suppressible nystagmus pattern described above, without hearing loss; labyrinthitis is the analogous process when hearing is also involved. The central causes that HINTS is designed to catch are a different problem altogether: cerebellar infarction, brainstem stroke, and demyelinating (multiple sclerosis) plaques.

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