Vertigo Classification and Clinical Guidelines

1. Classification by Anatomic Origin

Peripheral (Vestibular) Vertigo

• The American Academy of Otolaryngology–Head and Neck Surgery states that peripheral vertigo originates from the inner ear or vestibular apparatus. 1
• Positional triggers that provoke symptoms with head movement relative to gravity are characteristic of peripheral vertigo. 3
• Torsional nystagmus that fatigues with repeated testing helps identify peripheral disease. 5
• Absence of additional neurologic signs beyond vestibular symptoms distinguishes peripheral from central causes. 6
• Nystagmus that is suppressed by visual fixation is typical of peripheral vertigo. 7
• Benign paroxysmal positional vertigo (BPPV) is the most common peripheral disorder, accounting for roughly 42 % of vertigo presentations in primary‑care settings. 5
• Vestibular neuritis represents about 41 % of peripheral vertigo cases. 5
• Ménière’s disease accounts for ~10 % of primary‑care vertigo cases and up to 43 % in subspecialty clinics. 5
• Superior canal dehiscence syndrome and perilymph fistula are recognized peripheral etiologies, though prevalence data were not provided. 1

Central (CNS) Vertigo

• The American Academy of Otolaryngology–Head and Neck Surgery defines central vertigo as arising from brainstem, cerebellar, or other CNS pathology. 1
• Red‑flag ocular findings include down‑beating nystagmus on Dix‑Hallpike without a torsional component, direction‑changing nystagmus without head‑position changes, gaze‑evoked or direction‑switching nystagmus, and baseline nystagmus present without provocative maneuvers. 1
• Presence of additional neurologic deficits (e.g., dysarthria, dysmetria, dysphagia, sensory/motor loss, Horner’s syndrome) strongly suggests a central cause. 1
• Nystagmus that is not suppressed by visual fixation is a central feature. 7
• Brainstem or cerebellar stroke accounts for 10 % of cerebellar strokes that mimic peripheral vestibular disorders. 1
• Vestibular migraine has a lifetime prevalence of 3.2 % and explains about 14 % of all vertigo presentations. 1
• Vertebrobasilar insufficiency, multiple sclerosis, posterior fossa tumors, and central paroxysmal positional vertigo are additional central etiologies. [5][1]

2. Classification by Temporal Pattern (AAO‑HNS Guidelines)

Acute Vestibular Syndrome (AVS)

• Defined by continuous dizziness lasting days to weeks, accompanied by nausea, vomiting, and intolerance to head motion. 9
• Typical causes include vestibular neuritis, labyrinthitis, posterior‑circulation stroke, and demyelinating disease. 9

Triggered Episodic Vestibular Syndrome

• Episodes last seconds to < 1 minute and are provoked by specific actions, most often head or body position changes. 9
• Benign paroxysmal positional vertigo is the primary example, with posterior‑canal involvement in 85‑95 % of cases and lateral‑canal disease comprising the remainder. 3
• Differential diagnoses include postural hypotension and central paroxysmal positional vertigo. 7

Spontaneous Episodic Vestibular Syndrome

• Episodes last minutes to hours and occur without a specific trigger. 9
• Representative conditions:
  
  • Vestibular migraine (5 min–72 h; ≥5 episodes with migraine features). 1
  • Ménière’s disease (hours‑long attacks with fluctuating hearing loss, tinnitus, aural fullness). 9
  • Vertebrobasilar insufficiency (typically < 30 min). 6
  • Superior canal dehiscence (pressure‑triggered rather than position‑triggered). 1

Chronic Vestibular Syndrome

• Dizziness persists for weeks to months or longer, without a discrete episodic pattern. 9
• Common causes include anxiety/panic disorder, medication side effects, persistent postural‑perceptual dizziness, bilateral vestibulopathy, and cervicogenic vertigo. 9

3. Key Clinical Distinctions

Hearing‑Loss Patterns

• BPPV typically presents without any hearing loss. 3
• Ménière’s disease is characterized by fluctuating hearing loss accompanying vertigo attacks. 9
• Vestibular neuritis usually occurs without hearing loss. 8
• Labyrinthitis presents with profound hearing loss together with prolonged vertigo. 8

Response to Repositioning or Rehabilitation

• Lack of improvement after canalith repositioning procedures or vestibular rehabilitation should raise suspicion for a central etiology rather than BPPV. 1

Strength of evidence: The cited sources provide observational and epidemiologic data; specific grading (e.g., Class I‑III) was not reported in the referenced material.