Central and peripheral vertigo

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"vertigo"[MeSH Terms] AND "HINTS"

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peripheral versus central vertigo characteristics HINTS exam

Central vs peripheral vertigo

Key point: Vertigo can come from a lesion anywhere along the vestibular pathway. That pathway runs from the labyrinth to the vestibular nerve, then the vestibular nuclei and cerebellum, then the parietal cortex. Most cases are peripheral (inner ear). Central causes (brainstem or cerebellum) are less common, but some need emergency treatment, such as brainstem stroke or posterior fossa hemorrhage. - Neuroanatomy through Clinical Cases 3e, Ch. 12.6

Comparison

FeaturePeripheralCentral
OnsetSuddenGradual or sudden
IntensitySevere at first, then usually fadesUsually mild, but can be severe in stroke or MS
DurationBPPV: seconds to under 1 min. Vestibular neuritis: hours to daysWeeks to months, continuous. Can be seconds to minutes with posterior circulation TIA
NystagmusHorizontal or horizontal-torsional (neuritis). Upbeat-torsional (posterior canal BPPV). Direction is fixedPurely vertical, purely torsional, downbeating, or direction-changing on lateral gaze
Visual fixationSuppresses the nystagmusDoes not suppress it
Positional testingNystagmus is delayed, fatigues (habituates), and is prominent only when vertigo is presentNystagmus can be immediate, does not fatigue, and can be prominent without vertigo
Neurologic signsNoneUsually present
Auditory symptomsMay occur (tinnitus, hearing loss)Rare
Sources: ROSEN's Emergency Medicine, Table 15.3; Neuroanatomy through Clinical Cases 3e, Table 12.7; Cummings Otolaryngology (peripheral nystagmus suppresses with fixation).

Common causes

Peripheral
  • BPPV: brief (under 30 s), positional, fatigable episodes. The Dix-Hallpike test is positive for the posterior canal. The supine roll test is used for the horizontal canal.
  • Vestibular neuritis or labyrinthitis:
    • Vertigo develops over hours and subsides over days, sometimes after a viral illness.
    • Spontaneous nystagmus beats away from the lesion, and the head impulse test is positive.
    • Hearing is normal in neuritis. Hearing loss occurs in labyrinthitis.
  • Ménière disease: recurrent episodes lasting hours, with tinnitus, aural fullness and hearing loss. Hearing loss is required for the formal diagnosis.
  • Other causes: perilymphatic fistula, middle ear disease, barotrauma. - ROSEN's Emergency Medicine, Table 15.2
Central
  • Vertebrobasilar insufficiency or stroke: consider this in any older patient with new isolated vertigo and vascular risk factors. Associated features include headache, dysarthria, ataxia, diplopia, weakness and numbness. The neurologic exam may be normal early on.
  • Cerebellar hemorrhage: sudden severe onset with headache, vomiting and ataxia. Look for dysmetria and an ipsilateral sixth nerve palsy.
  • Wallenberg (lateral medullary) syndrome (PICA occlusion):
    • Loss of pain and temperature on the ipsilateral face and the contralateral body.
    • Hoarseness, palatal weakness and ipsilateral Horner syndrome.
  • Others: head trauma, multiple sclerosis, tumors (including cerebellopontine angle lesions), vestibular migraine, and drugs.
  • Central positional vertigo: this occurs with posterior fossa lesions. - Cummings Otolaryngology

Bedside approach

  1. Ask about red flags. Diplopia, dysarthria, weakness, sensory change, incoordination, or impaired consciousness mean posterior fossa disease until proven otherwise. Treat these urgently. - Neuroanatomy through Clinical Cases
  2. Check orthostatic vitals. A large drop in blood pressure or rise in pulse points to hypovolemia, drugs or cardiovascular causes rather than vestibular disease.
  3. Classify the syndrome by timing and triggers (this step comes from my own knowledge, not the retrieved textbook passages):
    • Episodic and triggered (BPPV).
    • Episodic and spontaneous (Ménière, vestibular migraine, TIA).
    • Acute continuous (neuritis versus stroke).
  4. Examine the eyes and gait.
    • In acute continuous vertigo with nystagmus, use the HINTS exam. Only trained examiners should do this, and only in patients who have nystagmus.
    • The findings that point to a central cause:
      • Head impulse test is normal (no catch-up saccade).
      • Nystagmus is direction-changing or vertical.
      • Skew deviation is present on the test of skew.
    • Inability to walk or sit unaided (truncal ataxia) is also a red flag for a central cause.
  5. Image when needed. MRI with diffusion-weighted imaging is the study of choice for suspected posterior circulation stroke. Early CT misses many of these strokes.

Recent evidence flag

A 2026 systematic review and meta-analysis of HINTS "family" tests (PMID 41045791) looked at diagnosing stroke in acute vestibular syndrome. I only saw the title and indexing data, not the abstract, so I can't say what accuracy figures it reports. Check it before relying on HINTS accuracy numbers. HINTS performance depends heavily on examiner expertise, and it is not valid in patients without nystagmus.

Memory aid

  • Peripheral: severe vertigo, horizontal fixed-direction nystagmus that suppresses with fixation, hearing symptoms, no neurologic signs, patient can walk.
  • Central: milder vertigo, vertical or direction-changing nystagmus that does not suppress, neurologic signs, severe imbalance.
I can go further on one area: BPPV maneuvers (Epley), the HINTS exam in detail, or vestibular migraine versus Ménière. Tell me which.
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