What are the causes of vertigo after herpes zoster infection?

Causes of Vertigo After Herpes Zoster

Vertigo after herpes zoster (shingles) results from direct viral invasion of the vestibular nerve (cranial nerve VIII) and/or the inner ear structures, with both the superior and inferior divisions of the vestibular nerve commonly affected. 1

Primary Mechanisms of Vestibular Damage

The varicella-zoster virus (VZV) causes vertigo through several distinct pathophysiological mechanisms:

Direct Vestibular Nerve Involvement

• Both superior and inferior divisions of the vestibular nerve within the internal auditory canal are affected in herpes zoster oticus (HZO) patients with vertigo 1
• Studies using caloric testing and vestibular evoked myogenic potential (VEMP) testing demonstrate that nerve trunks within the internal auditory canal are widely affected 1
• The virus can involve multiple cranial nerves simultaneously, including the 8th, 9th, and 10th cranial nerves 2

Inner Ear Infection

• Direct viral localization in the inner ear structures (labyrinthitis) causes acute vestibular dysfunction 3
• This manifests as sudden severe vertigo with profound hearing loss lasting more than 24 hours 4

Central Nervous System Complications

• Lateral medullary infarction can occur following VZV infection, presenting as isolated vertigo without other typical stroke symptoms 5
• VZV-associated vasculopathy causes small-vessel or large-vessel stroke syndromes affecting the brainstem or cerebellum 6
• CNS dissemination may involve brainstem structures, particularly in immunocompromised patients 7

Clinical Presentation Patterns

Herpes Zoster Oticus (HZO)

When vertigo occurs with HZO, expect:

• Auricular vesicles on the external ear (though onset of vertigo may precede visible vesicles)
• Facial palsy on the affected side (common association)
• Spontaneous nystagmus beating toward the healthy side
• Hearing loss (sensorineural) in approximately 60% of cases with vertigo 1
• Tinnitus and aural fullness 3

Timing and Duration

• Vertigo typically develops after the appearance of vesicles but can occasionally precede the rash 6
• Duration is usually prolonged (>24 hours), distinguishing it from benign peripheral causes 4
• Symptoms are not episodic or fluctuating like Ménière's disease 4

Bilateral Vestibular Involvement

Critical caveat: Rare cases demonstrate bilateral vestibular hypofunction from unilateral HZO 3. This occurs through:

• Autoimmune mechanisms triggered by the initial infection
• Contralateral vestibular loss developing days to weeks after initial presentation
• Only four such cases documented in literature 3

Post-COVID-19 Considerations

VZV reactivation following COVID-19 infection represents an emerging cause of vestibular dysfunction 8:

• COVID-19-induced immunosuppression and lowered cell-mediated immunity facilitates VZV reactivation
• Patients develop vertigo, hearing loss, tinnitus, and imbalance following shingles diagnosis post-COVID
• Peripheral vestibulopathy and otolith dysfunction documented on comprehensive balance testing 8

Distinguishing Features from Other Causes

Unlike other vestibular disorders:

• Permanent, non-fluctuating losses (vs. Ménière's disease which fluctuates) 4
• Associated with severe otalgia and fever (vs. vestibular neuritis) 4
• Prolonged vertigo >24 hours (vs. BPPV which lasts seconds) 4
• May lack typical stroke symptoms despite CNS involvement 5

Diagnostic Confirmation

When VZV-related vertigo is suspected:

• Cerebrospinal fluid PCR for VZV DNA provides definitive diagnosis 5
• Caloric testing shows absent or reduced response on affected side 1
• VEMP testing demonstrates absent responses indicating inferior vestibular nerve involvement 1
• Brain MRI may show gadolinium enhancement along nerve segments in the internal auditory canal or small infarcts in the dorsolateral medulla 5, 1
• Viral antibody titers (serum and CSF) show significant elevation 2

Important Clinical Pitfalls

1. Do not dismiss isolated vertigo in patients with facial herpes zoster—always screen for stroke with MRI 5
2. Perform lumbar puncture when neurological symptoms accompany HZO 5
3. Monitor for contralateral vestibular involvement in the weeks following initial presentation 3
4. Recognize that vesicles may be absent at time of presentation, particularly in cases of VZV vasculopathy 6