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Dizziness and Vertigo

Chapter 24 | Part 2 – Cardinal Manifestations & Presentation · Part 2 – Cardinal Manifestations & Presentation · Chapter 24

Key Clinical Points

  1. Dizziness is an imprecise term encompassing vertigo, light-headedness, faintness, and imbalance.
  2. Vertigo refers to a sense of spinning or other motion (physiological or pathological).
  3. Peripheral vestibular lesions cause unidirectional nystagmus with fast phases beating away from the lesion.
  4. Central vestibular lesions cause nystagmus that changes direction with gaze and is not suppressed by visual fixation.
  5. The head impulse test is the most useful bedside tool; a normal result makes an acute peripheral vestibular lesion unlikely.
  6. BPPV is caused by otoconia (calcium carbonate crystals) in semicircular canals, typically treated with repositioning maneuvers like the Epley maneuver.
  7. Vestibular neuritis usually recovers spontaneously; vestibular suppressants should be avoided after the first several days to allow central compensation.
  8. Ménière's disease is characterized by episodic vertigo, low-frequency hearing loss, and aural symptoms (pressure/fullness).
  9. Unilateral sensorineural hearing loss or vestibular hypofunction requires MRI of the internal auditory canals (with gadolinium) to rule out schwannoma.
  10. Bilateral vestibular hypofunction presents with imbalance in the dark and oscillopsia; treatment involves vestibular rehabilitation.

DEFINITION & OVERVIEW

• Dizziness: An imprecise term used to describe various sensations including vertigo, light-headedness, faintness, and imbalance. • Vertigo: ◦ Definition: Sense of spinning or other motion. ◦ Types: Can be physiological (e.g., during/after sustained head rotation) or pathological (vestibular dysfunction). • Light-headedness: ◦ Clinical Context: Classically refers to presyncopal sensations from brain hypoperfusion; however, patients may use it to describe other symptoms like disequilibrium. ◦ Presyncopal Causes: Include cardiac dysrhythmia, orthostatic hypotension, medication effects, or other causes of hypoperfusion. • Imbalance: Includes disequilibrium and oscillopsia (instability of vision when the head moves). • Peripheral Vestibular Disorders: ◦ Definition: Disorders affecting the labyrinths or vestibular nerves. • Central Vestibular Disorders: ◦ Definition: Result from disruption of central vestibular pathways.

EPIDEMIOLOGY

• Benign Paroxysmal Positional Vertigo (BPPV): A common cause of recurrent vertigo. • Vestibular Migraine: Common yet underdiagnosed; can present with episodic unilateral sensorineural hearing loss and vestibular hypofunction. • Bilateral Vestibular Hypofunction: May be idiopathic, progressive (part of a neurodegenerative disorder), or iatrogenic (e.g., from aminoglycoside antibiotics like gentamicin).

ETIOLOGY & PATHOPHYSIOLOGY

• Peripheral Vestibular Disorders: Affect the labyrinths or vestibular nerves. • Benign Paroxysmal Positional Vertigo (BPPV): ◦ Pathophysiology: Caused by free-floating otoconia (calcium carbonate crystals) dislodged from the utricular macula into semicircular canals, usually the posterior canal. • Vestibular Neuritis: ◦ Pathophysiology: Acute unilateral vestibular lesion → constant vertigo, nausea, vomiting, oscillopsia, and imbalance due to sudden asymmetry of inputs from the two labyrinths or their central connections, simulating continuous head rotation. • Vestibular Migraine: ◦ Pathophysiology: Vertigo may precede a typical migraine or occur without headache; motion sensitivity and sensitivity to visual motion are common. • Ménière's Disease: ◦ Pathophysiology: Associated with endolymphatic hydrops (excess endolymph fluid) in the inner ear. • Vestibular Schwannoma: ◦ Pathophysiology: Slowly progressive unilateral sensorineural hearing loss and vestibular hypofunction. ◦ Clinical Note: Patients typically do not have vertigo because the gradual deficit is compensated centrally as it develops. • Bilateral Vestibular Hypofunction: ◦ Pathophysiology: No asymmetry of vestibular input → patients do not experience vertigo, but suffer from imbalance and oscillopsia.

CLINICAL FEATURES

• Symptoms: Vertigo, nausea, vomiting, oscillopsia (motion of the visual scene), and imbalance. • Temporal Course: ◦ Seconds: BPPV; orthostatic hypotension (provoked by changes in head/body position). ◦ Minutes: Transient ischemic attacks (TIA) of the posterior circulation, migraine, or other causes. ◦ Hours: Vestibular migraine, Ménière's disease. ◦ Days: Vestibular neuritis, prolonged periods of disequilibrium in vestibular migraine.

DIFFERENTIAL DIAGNOSIS

• Peripheral vs. Central Distinction: Based on nystagmus characteristics, head impulse test (HIT) results, hearing loss, and associated neurologic signs. • Specific Conditions: ◦ BPPV: Brief episodes (<1 min), provoked by position changes. ◦ Vestibular Neuritis: Acute prolonged vertigo, spontaneous recovery. ◦ Vestibular Migraine: Episodic unilateral sensorineural hearing loss and vestibular hypofunction. ◦ Ménière's Disease: Vertigo, hearing loss, pain, pressure, fullness in affected ear. ◦ Vestibular Schwannoma: Slowly progressive unilateral sensorineural hearing loss. ◦ Bilateral Vestibular Hypofunction: Loss of balance (especially in the dark), oscillopsia. • Table 24-1: Features of Peripheral and Central Vertigo ◦ Nystagmus: → Peripheral: Unidirectional, fast phases beat away from the ear with the lesion; may be inhibited by visual fixation. → Central: Changes direction with gaze; not suppressed by visual fixation. ◦ BPPV Specifics: Transient mixed vertical-torsional nystagmus (pure vertical or pure torsional nystagmus is a central sign). ◦ Head Impulse Test: Absence of a head impulse sign in acute prolonged vertigo → suggests a central cause. ◦ Hearing/Neurology: → Unilateral hearing loss → suggests peripheral disorder. → Diplopia, dysarthria, and limb ataxia → suggest central disorder.

INVESTIGATIONS & DIAGNOSIS

  1. History: Assess for danger (arrhythmia, TIA/stroke), duration of episodes (seconds to days), and specific triggers.
  2. Physical Examination: ◦ Ocular Motility: Evaluate range, pursuit, saccades, cover test for vertical misalignment, and spontaneous nystagmus. ◦ Head Impulse Test: Assess VOR with small-amplitude (~20 degrees) rapid head rotations while patient fixates on a target. A normal result makes an acute peripheral lesion unlikely. ◦ Positioning Maneuvers: Dix-Hallpike (patient sits → head turned 45° toward affected ear → lowered to supine position with head extended back 20° while watching eyes).
  3. Ancillary Testing: ◦ Audiometry: Required for all suspected vestibular disorders. → Unilateral sensorineural hearing loss → supports peripheral (e.g., schwannoma). → Predominantly low-frequency hearing loss → characteristic of Ménière's disease. ◦ Videonystagmography (VNG): Records spontaneous and positional nystagmus. ◦ Caloric Testing: Compares responses of the two horizontal semicircular canals. ◦ Video Head-Impulse Test: Measures integrity of each of the six semicircular canals.
  4. Neuroimaging: ◦ MRI of Internal Auditory Canals (with gadolinium): Required for patients with unexplained unilateral hearing loss or vestibular hypofunction to rule out schwannoma.

MANAGEMENT & TREATMENT

  1. General Principle: Treatment must be driven by underlying diagnosis; avoid long-term use of vestibular suppressants as they may impede central compensation.
  2. Vestibular Neuritis: Most patients recover spontaneously; chronic dizziness, motion sensitivity, and disequilibrium may persist.
  3. Glucocorticoid Therapy: Efficacy is uncertain due to inconsistent study results.
  4. Antiviral Medications: No proven benefit; only used if evidence of Ramsay Hunt syndrome (herpes zoster oticus).
  5. Vestibular Suppressants: Use for acute symptoms only → avoid after first several days to allow central compensation.
  6. Vestibular Rehabilitation: Recommended for all patients to accelerate improvement and encourage return to normal activity.\
  7. Benign Paroxysmal Positional Vertigo (BPPV): Repositioning maneuvers (e.g., Epley maneuver) using gravity to move otoconia out of the semicircular canal.
  8. Ménière's Disease: Initial treatment includes diuretics and sodium restriction.
  9. Vestibular Schwannoma: MRI of internal auditory canals (with gadolinium); full ablative procedures are seldom required.\
  10. Bilateral Vestibular Hypofunction: Refer for vestibular rehabilitation.

PROGNOSIS & COMPLICATIONS

• Vestibular Neuritis: Spontaneous recovery common; chronic dizziness, motion sensitivity, and disequilibrium may persist. • Ménière's Disease: Hearing often improves between attacks, but permanent hearing loss may eventually occur. • Vestibular Schwannoma: Characterized by slowly progressive unilateral sensorineural hearing loss and vestibular hypofunction.

KEY PEARLS & CLINICAL TRAPS

• Board Exam Favorites: → Head impulse test. → Nystagmus direction (unidirectional vs. gaze-evoked). → Fixation suppression (peripheral vs. central). • Clinical Traps: → Long-term use of vestibular suppressants → delays recovery by hindering central compensation. • Diagnostic Pitfalls: → A central lesion cannot always be ruled out by exam alone; older patients with vascular risk factors who present with an acute vestibular syndrome must be evaluated for the possibility of stroke even when there are no specific findings that indicate a central lesion.

FLOWCHARTS

Modified Epley Maneuver (Treatment of BPPV)

Step 1: Patient seated → turn head 45 degrees toward the affected ear. Step 2: Keep head turned → lower to head-hanging position → hold ≥ 30 s until nystagmus disappears. Step 3: Without lifting head → turn it 90 degrees toward the other side → hold for 30 s. Step 4: Rotate patient onto their side while turning head another 90 degrees (nose pointed down 45 degrees) → hold for 30 s. Step 5: Patient sits up on the side of the table → rest briefly → repeat maneuver to confirm success.

Reference Tables

TABLE 24-1 Features of Peripheral and Central Vertigo • Nystagmus from an acute peripheral lesion is unidirectional…

Harrison's 22e, p.163

  • • Nystagmus from an acute peripheral lesion is unidirectional, with fast phases
    beating away from the ear with the lesion. Nystagmus that changes direction
    with gaze is due to a central lesion.
    • Transient mixed vertical-torsional nystagmus occurs in benign paroxysmal
    positional vertigo (BPPV), but pure vertical or pure torsional nystagmus is a
    central sign.
    • Nystagmus from a peripheral lesion may be inhibited by visual fixation,
    whereas central nystagmus is not suppressed.
    • Absence of a head impulse sign in a patient with acute prolonged vertigo
    should suggest a central cause.
    • Unilateral hearing loss suggests peripheral vertigo. Findings such as diplopia,
    dysarthria, and limb ataxia suggest a central disorder.