Vestibular Neuronitis: Cause and Treatment
Etiology
Vestibular neuronitis is caused by reactivation of herpes simplex virus type 1 that affects the vestibular ganglion, vestibular nerve, or labyrinth. 1, 2, 3
- The condition results in acute unilateral loss of vestibular function, preferentially involving the superior vestibular labyrinth and its afferents 3
- The posterior semicircular canal and saccule (inferior vestibular labyrinth) are typically spared, though a rare inferior vestibular neuritis subtype exists 3
Critical Diagnostic Caveat
Before diagnosing vestibular neuronitis, you must exclude posterior circulation stroke—approximately 25% of acute vestibular syndrome presentations are caused by stroke, rising to 75% in high vascular-risk patients. 4
- Any patient with significant cardiovascular risk factors presenting with acute vestibular syndrome requires evaluation for stroke 5, 1
- Red flags demanding immediate MRI include: severe postural instability with falling, new-onset severe headache, any additional neurological symptoms, downbeating nystagmus without torsional component, or failure to respond to treatment 5, 6
- Up to 80% of stroke-related acute vestibular syndrome patients lack focal neurologic deficits 4
Acute Phase Treatment (First 3-5 Days)
Corticosteroids
Methylprednisolone significantly improves recovery of peripheral vestibular function and should be initiated within 24 hours of symptom onset for maximum benefit. 2, 7
- All patients (100%) treated within 24 hours achieved normal caloric test results at 3 months, compared to only 58% treated between 25-72 hours 7
- Standard regimen: oral prednisolone 50 mg daily for 5 days, then taper over the next 5 days 7
- If severe nausea/vomiting: add intravenous betamethasone 8 mg for the first 1-2 days 7
- Withhold steroids in patients at higher risk of steroid complications 1
Antiviral Therapy
Valacyclovir provides no benefit and should not be used. 2
- A randomized controlled trial demonstrated valacyclovir had no effect on vestibular function recovery (P=0.43) 2
- Combination therapy (methylprednisolone plus valacyclovir) was not superior to corticosteroid monotherapy 2
Symptomatic Medications
Antiemetics and vestibular suppressants should be used only during the first several days, then discontinued immediately to avoid delaying central compensation. 5, 1
- Prolonged use of vestibular suppressants interferes with the brain's natural compensation mechanisms and causes significant adverse effects 5
- Benzodiazepines should be avoided entirely due to impaired central vestibular compensation, increased fall risk, and cognitive dysfunction 5
Recovery Phase (After Acute Phase)
Early Mobilization
Encourage immediate resumption of normal activity as soon as the acute phase resolves to promote central compensation. 1
- Recovery occurs through central compensation, which is impaired by vestibular suppressants and enhanced by early mobilization 5
Vestibular Rehabilitation
Directed vestibular rehabilitation therapy should be initiated to accelerate recovery and promote central compensation. 1, 3
- Vestibular rehabilitation hastens recovery beyond natural compensation 3
Follow-Up
Reassess patients within 1 month after initial treatment to document resolution or persistence of symptoms. 5
- Persistent symptoms, unprecedented headache, negative head impulse test, severe unsteadiness, or no recovery within 1-2 days warrant brain imaging 3
Common Pitfalls to Avoid
- Do not continue vestibular suppressants beyond the acute phase—this is the most critical error, as prolonged use significantly delays recovery 5, 1
- Do not delay steroid treatment—efficacy drops dramatically after 24 hours 7
- Do not miss posterior circulation stroke—maintain high suspicion in patients with vascular risk factors, even without focal neurologic signs 4, 1
- Do not prescribe valacyclovir—it has been proven ineffective 2