Bedside Vestibular Examination

The bedside vestibular examination is the single most important tool for evaluating acute vertigo — more sensitive than early MRI for detecting posterior fossa stroke, more cost-effective than any laboratory test, and immediately available. A structured approach using the HINTS Plus examination can distinguish peripheral from central vestibular syndromes with sensitivity exceeding 96% for stroke, outperforming initial DWI-MRI which has a false-negative rate of 15–20% for small cerebellar infarctions in the first 48 hours. Beyond the acute vestibular syndrome, bedside testing with Dix-Hallpike, supine roll, gait assessment, and systematic nystagmus evaluation allows accurate diagnosis of BPPV, characterization of nystagmus patterns, and identification of vestibular hypofunction — often without requiring any laboratory testing at all. Mastering these techniques is essential for every neurologist.

The HINTS Plus Examination

The HINTS examination (Kattah et al., 2009) is designed specifically for the acute vestibular syndrome (AVS) — defined as acute-onset continuous vertigo/dizziness with nystagmus, nausea/vomiting, head-motion intolerance, and gait unsteadiness lasting hours to days. It should NOT be applied to episodic or chronic dizziness presentations.

Head Impulse Test (HIT)

Nystagmus Evaluation

Test of Skew (Alternate Cover Test)

• Technique: Patient fixates on examiner’s nose; examiner alternately covers and uncovers each eye, observing for vertical re-fixation movement of the uncovered eye
• Positive test (skew deviation): Vertical correction — the uncovered eye moves vertically to re-fixate; indicates misalignment of the otolithic-ocular pathways
• Interpretation: Skew deviation in AVS is a central finding, indicating a brainstem lesion; it has high specificity (~98%) but moderate sensitivity (~30%) for stroke
• Key point: Even small amounts of vertical misalignment are significant; if uncertain, repeat several times and observe closely

Hearing Assessment (HINTS Plus)

HINTS Interpretation Summary

Dix-Hallpike Maneuver

Technique (Step-by-Step)

1. Patient seated on exam table, positioned so that when supine, the head will extend beyond the edge of the table
2. Turn the patient’s head 45° to the side being tested (e.g., right ear for right posterior canal)
3. Rapidly bring the patient from seated to supine with the head hanging approximately 20–30° below horizontal, maintaining the 45° head turn throughout
4. Observe the eyes closely for nystagmus; maintain position for at least 30–60 seconds
5. Return the patient to the seated position and observe for reversal nystagmus
6. Allow at least 1–2 minutes before testing the opposite side (to avoid additive effects)

Interpretation: Posterior Canal BPPV

Supine Roll Test (Horizontal Canal BPPV)

• Indication: Suspected horizontal (lateral) canal BPPV; patient reports positional vertigo with rolling in bed; second most common form of BPPV (~15–30% of BPPV cases)
• Technique:
  • Patient supine with head elevated ~20° (pillow under head) to bring the horizontal canal into the vertical plane
  • Rapidly turn the head 90° to one side; observe for horizontal nystagmus; note direction and intensity
  • Return to neutral; wait for nystagmus to resolve (at least 30 seconds)
  • Rapidly turn the head 90° to the opposite side; observe for horizontal nystagmus
  • Compare intensity of nystagmus in both directions
• Geotropic pattern: Nystagmus beats toward the ground in both positions; stronger side = affected side; indicates free-floating otoconia in the posterior arm of the horizontal canal (canalithiasis); nystagmus is transient, decrescendo; treated with Lempert (BBQ roll) or Gufoni maneuver
• Apogeotropic pattern: Nystagmus beats away from the ground in both positions; weaker side = affected side; indicates otoconia attached to the cupula (cupulolithiasis) or in the anterior arm of the canal; nystagmus may be more persistent; treated with Gufoni maneuver (for apogeotropic variant) or head-shaking/forced prolonged position
• Key distinction from central positional nystagmus: Horizontal canal BPPV produces direction-changing positional nystagmus (which can appear “central”), but the geotropic/apogeotropic pattern with asymmetric intensity is the diagnostic clue; if nystagmus is symmetric or does not fit either pattern, consider central pathology

Anterior Canal BPPV

• Prevalence: Rare (<3–5% of BPPV cases); some authorities question whether true anterior canal BPPV exists, as the anatomy makes canalith trapping less likely
• Dix-Hallpike response: Downbeat nystagmus with torsional component beating toward the opposite (upper) ear — this is the mirror image of posterior canal BPPV nystagmus
• Clinical challenge: Downbeat nystagmus on Dix-Hallpike is more commonly central than peripheral; anterior canal BPPV should only be diagnosed after MRI has excluded a posterior fossa lesion
• Treatment: Reverse Epley maneuver or prolonged head-hanging position; resolution is typically rapid

Gait and Balance Assessment

Nystagmus Assessment Techniques

Fixation and Frenzel Goggles

• Principle: Visual fixation suppresses peripheral vestibular nystagmus (because the visual system can override the vestibular imbalance) but does NOT suppress central nystagmus (because the central pathways mediating suppression are themselves damaged)
• Frenzel goggles: +20 diopter lenses that blur the patient’s vision, eliminating visual fixation while magnifying the eyes for the examiner; the gold standard for removing fixation at the bedside
• Alternatives to Frenzel goggles: Observe the optic disc with an ophthalmoscope (disc moves in the direction of the slow phase — opposite to the conventionally observed fast phase direction); cover the non-examined eye
• Clinical application: If nystagmus increases when fixation is removed (Frenzel goggles) → peripheral; if nystagmus is unchanged or increases with fixation → central

Head-Shaking Nystagmus

• Technique: Patient closes eyes; examiner oscillates the head horizontally (~2 Hz) for 15–20 seconds; observe for nystagmus immediately after stopping
• Interpretation:
  • Horizontal nystagmus (fast phase away from lesion) → unilateral peripheral vestibular hypofunction (velocity storage asymmetry)
  • Vertical nystagmus (downbeat) after horizontal head shaking → central (cerebellar) pathology — highly specific
  • Absent nystagmus → normal or symmetric vestibular function
• Clinical utility: Useful for detecting latent vestibular asymmetry that is not apparent on spontaneous nystagmus examination; a “cross-coupled” response (vertical nystagmus from horizontal shaking) is a red flag for central pathology

Dynamic Visual Acuity Test (DVAT)

• Purpose: Assesses VOR function at the bedside by measuring the degradation of visual acuity during head movement
• Technique:
  • Measure best corrected visual acuity on a Snellen chart (static baseline)
  • Oscillate the patient’s head passively at ~2 Hz in the horizontal plane
  • Measure visual acuity again during head oscillation
• Interpretation: Loss of ≥3 lines on the Snellen chart indicates VOR hypofunction (the VOR is not adequately stabilizing gaze during head movement); loss of ≤1 line is normal
• Clinical utility: Quantifies the functional impact of VOR loss; useful for monitoring recovery in vestibular neuritis and bilateral vestibulopathy; can detect bilateral vestibular hypofunction that may not be apparent on HIT

Hyperventilation-Induced Nystagmus

• Technique: Patient hyperventilates vigorously for 30–60 seconds; observe for nystagmus (with Frenzel goggles ideally)
• Interpretation:
  • Nystagmus toward the affected side → demyelinating lesion of CN8 (e.g., MS plaque at the root entry zone); hyperventilation-induced alkalosis improves conduction in demyelinated fibers, transiently restoring excitability and producing an imbalance
  • Nystagmus away from the affected side → vestibular schwannoma; hyperventilation-induced alkalosis may enhance excitability of compressed (but intact) fibers
  • Absent response → normal (or non-demyelinating vestibular pathology)
• Clinical utility: Helps distinguish vestibular schwannoma from demyelinating vestibular neuropathy; supports the need for MRI with IAC protocol
• Caveat: Hyperventilation can itself produce dizziness (lightheadedness from hypocapnia) and anxiety; the test specifically looks for nystagmus, not dizziness symptoms

Vibration-Induced Nystagmus

• Technique: Apply a vibrating device (e.g., 100 Hz tuning fork or handheld massager) to the mastoid process on each side; observe for nystagmus with Frenzel goggles
• Interpretation: Vibration asymmetrically stimulates the vestibular organs; nystagmus beating away from the affected side indicates unilateral vestibular hypofunction
• Sensitivity: ~70–80% for detecting unilateral vestibular loss; less sensitive than caloric testing but quick and easy to perform
• Clinical utility: Rapid screening test for unilateral vestibular hypofunction in the outpatient setting; particularly useful when caloric testing is not immediately available

Valsalva-Induced Nystagmus (Tullio/Hennebert Phenomenon)

• Technique: Patient performs Valsalva maneuver against a closed glottis, or the examiner applies positive/negative pressure to the ear canal (pneumatic otoscopy/tragal compression); observe for vertigo and nystagmus
• Interpretation:
  • Nystagmus provoked by pressure changes or loud sounds (Tullio phenomenon) → superior semicircular canal dehiscence syndrome (SCDS)
  • SCDS creates a “third window” in the bony labyrinth, making the vestibular end organs abnormally sensitive to pressure and sound
  • The nystagmus direction depends on the affected canal (typically vertical-torsional, in the plane of the dehiscent superior canal)
• Associated findings in SCDS: Autophony (hearing own voice, heartbeat, or eye movements), conductive hyperacusis, low-frequency air-bone gap on audiometry with normal tympanometry, enhanced VEMPs with low threshold
• Confirmation: High-resolution CT of the temporal bone (0.5 mm cuts) to visualize the dehiscence; VEMPs (enhanced cVEMP/oVEMP with decreased threshold)

Clinical Algorithm: Approach Based on Timing and Triggers

Comprehensive Bedside Test Reference

Practical Pearls

Common Pitfalls and Misdiagnoses

Emergency Department Vestibular Assessment

Repositioning Maneuvers

While not strictly part of the “diagnostic” bedside exam, repositioning maneuvers are performed immediately after a positive Dix-Hallpike or supine roll test and are integral to the bedside vestibular assessment.

Epley Maneuver (Canalith Repositioning Procedure)

• Indication: Positive Dix-Hallpike for posterior canal BPPV
• Technique:
  1. Begin from the positive Dix-Hallpike position (head hanging, turned 45° toward affected ear)
  2. Rotate the head 90° to the opposite side (now head is turned 45° toward the unaffected ear, still hanging)
  3. Roll the patient onto their side (face toward the floor), rotating the head an additional 90°
  4. Slowly sit the patient up from the side-lying position
  5. Hold each position for ~30–60 seconds or until nystagmus resolves
• Efficacy: Resolution of BPPV in 70–80% after a single session; >90% after 2–3 sessions
• Post-maneuver instructions: Controversy exists about post-procedure restrictions (sleeping upright, avoiding affected side); evidence suggests restrictions do NOT improve outcomes and are no longer routinely recommended

Lempert (BBQ Roll) Maneuver

• Indication: Geotropic horizontal canal BPPV (positive supine roll test)
• Technique: Sequential 90° head turns from the affected ear down, through supine, to the unaffected ear down, face down, and back to the starting position (360° roll toward the unaffected side); each position held for 30–60 seconds
• Alternative: Gufoni maneuver (rapid side-lying technique) is faster and well-tolerated

References

1. Kattah JC, Talkad AV, Wang DZ, Hsieh YH, Newman-Toker DE. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009;40(11):3504–3510.
2. Newman-Toker DE, Curthoys IS, Halmagyi GM. Diagnosing stroke in acute vertigo: the HINTS family of eye movement tests and the future of the “Eye ECG.” Semin Neurol. 2015;35(5):506–521.
3. Halmagyi GM, Curthoys IS. A clinical sign of canal paresis. Arch Neurol. 1988;45(7):737–739.
4. Dix MR, Hallpike CS. The pathology, symptomatology and diagnosis of certain common disorders of the vestibular system. Proc R Soc Med. 1952;45(6):341–354.
5. Tarnutzer AA, Berkowitz AL, Robinson KA, Hsieh YH, Newman-Toker DE. Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome. CMAJ. 2011;183(9):E571–E592.
6. Edlow JA, Gurley KL, Newman-Toker DE. A new diagnostic approach to the adult patient with acute dizziness. J Emerg Med. 2018;54(4):469–483.
7. Bhattacharyya N, Gubbels SP, Schwartz SR, et al. Clinical practice guideline: benign paroxysmal positional vertigo (update). Otolaryngol Head Neck Surg. 2017;156(3 Suppl):S1–S47.
8. Hain TC, Helminski JO. Anatomy and physiology of the normal vestibular system. In: Herdman SJ, Clendaniel R, eds. Vestibular Rehabilitation. 4th ed. F.A. Davis; 2014:2–19.
9. Saber Tehrani AS, Kattah JC, Mantokoudis G, et al. Small strokes causing severe vertigo: frequency of false-negative MRIs and nonlacunar mechanisms. Neurology. 2014;83(2):169–173.
10. Mantokoudis G, Saber Tehrani AS, Kattah JC, et al. Quantifying the vestibulo-ocular reflex with video-oculography: nature and frequency of artifacts. Audiol Neurootol. 2015;20(1):39–50.
11. Young AS, Nham B, Bradshaw AP, Calic Z, Halmagyi GM, McGarvie LA. Clinical, oculographic, and vestibular test characteristics of vestibular migraine. Cephalalgia. 2021;41(10):1039–1052.
12. Lee SH, Kim JS. Benign paroxysmal positional vertigo. J Clin Neurol. 2010;6(2):51–63.
13. Choi JY, Kim JS. Nystagmus and central vestibular disorders. Curr Opin Neurol. 2017;30(1):98–106.
14. Kerber KA, Newman-Toker DE. Misdiagnosing dizzy patients: common pitfalls in clinical practice. Neurol Clin. 2015;33(3):565–575.