# Vestibular Assessment and Benign Paroxysmal Positional Vertigo
## Overview
Vestibular disorders are among the most common complaints in otolaryngology. A systematic approach to the dizzy patient, differentiating peripheral from central vertigo, is essential. BPPV is the most common cause of vertigo and is readily treated with canalith repositioning maneuvers.
## Vestibular Anatomy Review
Three semicircular canals (SCCs): lateral (horizontal), superior (anterior), posterior -- detect angular acceleration. Otolith organs: utricle (horizontal linear acceleration) and saccule (vertical linear acceleration/gravity). Vestibular nerve: superior division (lateral SCC, superior SCC, utricle) and inferior division (posterior SCC, saccule). Vestibulo-ocular reflex (VOR): stabilizes gaze during head movement; 3-neuron arc from vestibular nerve to CN III/IV/VI nuclei to extraocular muscles.
## Approach to the Dizzy Patient
### History -- Key Questions
Character: true vertigo (spinning) vs. lightheadedness, imbalance, presyncope. Duration of episodes: seconds (BPPV), minutes-hours (Meniere), days (vestibular neuritis), constant. Triggers: positional (BPPV), head movement, Valsalva, loud noise (superior SCC dehiscence). Associated symptoms: hearing loss, tinnitus, aural fullness (Meniere), headache (migraine), neurologic symptoms (central). Medications: vestibulotoxic drugs.
### Peripheral vs. Central Vertigo
| Feature | Peripheral | Central |
|---------|-----------|---------|
| Onset | Sudden, episodic | Gradual or sudden |
| Nystagmus | Unidirectional, horizontal-torsional, suppressed by fixation | Direction-changing, purely vertical, not suppressed |
| Hearing loss | Often present | Uncommon |
| Neurologic signs | Absent | Present (diplopia, dysarthria, dysphagia, weakness) |
| Duration | Seconds to days | Variable |
| Imbalance severity | Mild-moderate | Severe (unable to walk) |
## Office-Based Vestibular Examination
### Spontaneous Nystagmus
Observe in primary gaze, then with fixation removed (Frenzel goggles or infrared video goggles). Peripheral: unidirectional, enhanced without fixation. Alexander law: peripheral nystagmus increases when looking in the direction of the fast phase.
### Head Impulse Test (HIT)
Tests VOR; rapid passive head turn to each side while patient fixates on examiner's nose. Positive (corrective saccade) = peripheral vestibular hypofunction on the side of the head turn. A normal HIT with acute vertigo and nystagmus suggests central pathology (stroke) -- part of HINTS exam.
### HINTS Examination (Head Impulse, Nystagmus, Test of Skew)
Used to differentiate peripheral vestibular neuritis from posterior fossa stroke in acute vestibular syndrome. **Peripheral (vestibular neuritis)**: positive HIT, unidirectional nystagmus, no skew deviation. **Central (stroke)**: normal HIT, direction-changing nystagmus, skew deviation present. HINTS is more sensitive than early MRI for posterior fossa stroke.
### Dix-Hallpike Test
Diagnostic test for posterior canal BPPV (most common form). Patient seated, head turned 45 degrees to the tested side, rapidly laid supine with head hanging 20 degrees below the table. Positive: upbeating torsional nystagmus (geotropic, toward the affected ear) with latency (2-5 seconds), crescendo-decrescendo, duration <60 seconds, fatigable. The affected ear is the downward ear when nystagmus is provoked.
### Supine Roll Test (Pagnini-McClure)
Diagnostic for lateral (horizontal) canal BPPV, Patient supine, head turned rapidly to each side. Geotropic nystagmus (toward the ground) = canalolithiasis of the lateral canal (affected side has more intense nystagmus). Apogeotropic nystagmus (away from the ground) = cupulolithiasis variant (affected side has less intense nystagmus).
### Other Bedside Tests
**Fukuda stepping test**: patient marches in place with eyes closed; rotation >30 degrees toward one side suggests ipsilateral vestibular hypofunction. **Romberg test**: standing balance with eyes closed; fall toward hypofunction side. **Dynamic visual acuity**: visual acuity drops >2 lines with head oscillation suggests bilateral vestibular hypofunction.
## Vestibular Function Testing
### Electronystagmography (ENG) / Videonystagmography (VNG)
Evaluates vestibular function via eye movement recording (electrodes or infrared cameras). Components: **Oculomotor testing**: saccades, smooth pursuit, optokinetic nystagmus (abnormal = central). **Positional/positioning testing**: identifies nystagmus with position changes. **Caloric testing**: warm (44C) and cool (30C) water/air irrigation of each ear; measures lateral SCC function. Unilateral weakness >20-25% = peripheral hypofunction on the weak side. Mnemonic: COWS (Cold Opposite, Warm Same -- direction of nystagmus fast phase). Bilateral caloric weakness suggests bilateral vestibular loss (ototoxicity, bilateral Meniere).
### Rotary Chair Testing
Tests VOR across range of frequencies. Useful for bilateral vestibular loss, monitoring vestibular compensation, and central vs. peripheral differentiation. Measures gain, phase, and symmetry of VOR.
### Vestibular Evoked Myogenic Potentials (VEMPs)
**cVEMP** (cervical): inhibitory response in SCM muscle; tests saccular/inferior vestibular nerve function. Abnormal in superior SCC dehiscence (enhanced/lowered threshold), Meniere disease, vestibular schwannoma. **oVEMP** (ocular): excitatory response in inferior oblique; tests utricular/superior vestibular nerve function. Enhanced in superior SCC dehiscence.
### Video Head Impulse Test (vHIT)
Quantitative measurement of VOR gain for each semicircular canal. Identifies covert saccades not visible on clinical HIT. Gain <0.8 with corrective saccades = hypofunction of the tested canal.
## Benign Paroxysmal Positional Vertigo (BPPV)
### Pathophysiology
**Canalolithiasis** (most common): free-floating otoconia (calcium carbonate crystals from utricle) in the SCC, creating endolymph displacement with position change. **Cupulolithiasis**: otoconia adherent to the cupula, making it gravity-sensitive. Most commonly affects the **posterior canal** (85-90%), then **lateral canal** (10-15%), rarely **superior canal** (<1%).
### Epidemiology
Most common cause of vertigo; lifetime prevalence ~2.4%, Peak incidence in 5th-7th decade. Female predominance (2:1). Risk factors: head trauma, prolonged bed rest, osteoporosis, vitamin D deficiency, inner ear disease (post-labyrinthitis, post-Meniere).
### Clinical Presentation
Brief episodes (10-30 seconds) of vertigo triggered by specific head positions. Rolling over in bed, looking up, bending over, Nausea common; vomiting less common, No hearing loss, tinnitus, or neurologic symptoms, Periods of remission and recurrence.
### Treatment
#### Posterior Canal BPPV
**Epley maneuver (canalith repositioning procedure)**: treatment of choice. Dix-Hallpike position on affected side (provoke nystagmus). Wait for nystagmus to resolve. Turn head 90 degrees to the opposite side (keeping head hanging). Roll body to same side (nose facing floor). Slowly sit up. Success rate: 80-90% with 1-2 treatments. **Semont maneuver**: alternative; rapid side-to-side movement. Post-treatment position restrictions: controversial and likely unnecessary.
#### Lateral Canal BPPV
**Geotropic type (canalolithiasis)**: **Lempert (BBQ roll)**: 360-degree roll away from the affected ear in 90-degree increments. **Gufoni maneuver**: rapid side-lying to the unaffected side, then rapid head rotation toward the floor. **Apogeotropic type (cupulolithiasis)**: Gufoni maneuver (toward affected side, head up). Head-shaking, or forced prolonged position.
### Recurrence
Recurrence rate: ~15% per year; up to 50% over 5 years. Consider vitamin D supplementation if deficient (RCT evidence for reduced recurrence). Refractory BPPV (rare): posterior canal plugging surgery.
Step-by-step illustration of the Dix-Hallpike test and Epley canalith repositioning maneuver for right posterior canal BPPV. Sequential panels showing: (1) patient seated with head turned 45 degrees right, (2) rapidly laid supine with head hanging off table edge showing upbeating torsional nystagmus, (3) head turned 90 degrees to the left, (4) patient rolled onto left side with nose toward floor, (5) patient brought to sitting position. Inset diagrams showing otoconia position in the posterior semicircular canal at each step.
Diagram of the three semicircular canals (posterior, lateral, superior) with otoconia shown in the posterior canal lumen causing canalolithiasis. The cupula, ampulla, utricle, and endolymphatic flow direction during head movement are labeled. Comparison panel showing cupulolithiasis variant with otoconia attached to the cupula. Anatomical cross-section illustration.
HINTS examination protocol illustration showing three components: (1) Head Impulse Test with examiner performing rapid head turn and patient showing corrective saccade (peripheral positive), (2) Nystagmus assessment showing unidirectional horizontal nystagmus (peripheral) vs direction-changing (central), (3) Test of Skew showing cover-uncover test with vertical realignment (central positive). Three-panel clinical examination diagram.
## Clinical Pearls
BPPV is the most common cause of vertigo and is diagnosed clinically -- no imaging or vestibular testing needed in straightforward cases. The Epley maneuver is curative in 80-90% of posterior canal BPPV cases and can be repeated at the same visit if initially unsuccessful. A positive HINTS exam (positive HIT, unidirectional nystagmus, no skew) in acute vestibular syndrome is more sensitive than early MRI for ruling out posterior fossa stroke. Caloric testing only assesses lateral canal function at a very low frequency; it does not test the entire vestibular system. Nystagmus that changes direction with gaze, is purely vertical, or is not suppressed by visual fixation should be considered central until proven otherwise. Lateral canal BPPV produces horizontal nystagmus on the supine roll test; geotropic = canalolithiasis (more common), apogeotropic = cupulolithiasis. Vitamin D deficiency is associated with BPPV recurrence; check and supplement if low. Vestibular suppressants (meclizine, benzodiazepines) should be used sparingly and short-term as they impair central vestibular compensation.
## References
- 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.
- Kattah JC, Talkad AV, Wang DZ, et al. "HINTS to diagnose stroke in the acute vestibular syndrome." *Stroke*. 2009;40(11):3504-3510.
- Jeong SH, Kim HJ, Kim JS. "Vestibular neuritis." *Semin Neurol*. 2013;33(3):185-194.
- Parnes LS, Agrawal SK, Atlas J. "Diagnosis and management of benign paroxysmal positional vertigo (BPPV)." *CMAJ*. 2003;169(7):681-693.