Definition and Overview
Vestibular neuritis is an acute peripheral vestibular disease in which inflammation occurs in the vestibular nerve (vestibular branch of the 8th cranial nerve) that connects the inner ear and the brain, causing sudden and severe rotary vertigo. The hearing nerve is preserved and is characterized by no hearing loss.
It is the third most common cause of acute vertigo, with an annual incidence of approximately 3.5 per 100,000 people. It occurs at any age, but is most prevalent in those in their 30s to 60s and has seasonal fluctuations.
cause
Viral infection is believed to be the main cause. There is a case report in which herpes simplex virus-1 (HSV-1) DNA was detected in a biopsy of the vestibular nerve, and the most likely hypothesis is that reactivation after latent infection causes vestibular neuritis.
Clinically, it often occurs after upper respiratory infection or influenza, suggesting a strong correlation with viral infection. Autoimmune mechanisms or microscopic blood flow disorders may also be involved in some cases.
symptoms
Acute phase (1-3 days)
- Sudden, severe rotatory vertigo: starts in a few minutes and lasts for several days. Dizziness occurs even when standing still and worsens with movement.
- Nausea and Vomiting: Severe dizziness causes repeated vomiting.
- Spontaneous nystagmus: Horizontal-circular nystagmus that pulsates in the direction opposite to the affected side.
- Gait instability: A gait disorder that leans toward the affected side occurs.
- Hearing preservation: The difference from Meniere's disease is that it is not accompanied by hearing loss and tinnitus.
Recovery period (days to weeks)
Acute dizziness gradually decreases and walking becomes possible, but instability persists during rapid head movements. Reduced response to head movement on the side with vestibular function loss (reduced vestibulo-ocular reflex) persists.
Aftereffects
- Secondary otolithiasis (BPPV): Otolithiasis occurs in approximately 10% of cases after vestibular neuritis.
- Persistent postural-perceptual dizziness (PPPD): There are cases where psychological factors are added after vestibular neuritis, resulting in chronic dizziness.
diagnosis
Video Head Impulse Test (vHIT)
A corrective saccade (catch-up saccade) was observed during head impulse of the semicircular canal on the affected side, confirming a decrease in vestibulo-ocular reflex function. It is a key test in differentiating vestibular neuritis and stroke.
In stroke-related vertigo, the head impulse test is normal (H in the HINTS test protocol), suggesting a central cause.
Video nystagmus test
Record the direction, intensity, and changes in gaze of spontaneous nystagmus. In vestibular neuritis, horizontal-rotating spontaneous nystagmus toward the unaffected side appears and gaze suppression is possible. Central nystagmus is variable in direction and does not inhibit gaze.
Caloric test
The vestibular function of both sides is compared by injecting hot and cold water into the external auditory canal. If the response of the semicircular canal on the affected side is significantly lower than that on the healthy side (Canal Paresis > 25%), unilateral vestibular dysfunction is diagnosed.
brain MRI
Diffusion-weighted MRI (DWI) is performed to rule out central causes such as stroke or cerebellar hemorrhage. However, clinical judgment is important as cerebellar infarction may not be detected on DWI within the first 48 hours.
treatment
Acute symptom control
- Anti-vertigo drugs (meclizine, dimenhydrinate): Relieve dizziness in the acute phase.
- Antiemetics (metoclopramide, ondansetron): Control of nausea and vomiting.
- Benzodiazepines: short-term use in the acute phase. Long-term use disrupts vestibular compensation.
The drug is used only in the acute phase (several days). Continued use of the drug may delay the central compensation process.
steroid treatment
There are studies showing that initial methylprednisolone (taper from 100 mg) promotes vestibular function recovery. The rule is to start within 48 to 72 hours after symptoms appear. However, evidence on long-term functional outcomes is limited.
vestibular rehabilitation exercise
Vestibular rehabilitation exercise is the most important long-term treatment in the recovery of vestibular neuritis. According to a Cochrane systematic literature review, vestibular rehabilitation significantly improves dizziness, balance, and quality of life in unilateral peripheral vestibular dysfunction.
Cawthorne-Cooksey Athletic Program: - Stage 1 (recumbent position): eye movement, head movement - Stage 2 (sitting position): head-eye coordination exercises, balance training - Stage 3 (standing position): training to reduce dependence on vision, gait training - Stage 4 (on the move): Combined gaze stabilization and gait training
Gaze stabilization exercise: Retrain the vestibulo-ocular reflex function by watching a stationary target against a moving background or fixing the target while moving the head.
Progress and prognosis
Vestibular neuritis usually has a good prognosis. After the acute phase, central compensation occurs over several weeks to several months, and symptoms improve.
Full recovery of vestibular function occurs in approximately 50% of cases, while partial recovery or loss of function persists in the remainder. However, in most cases, central compensation recovers to a level that does not interfere with daily life.
Poor prognostic factors: older age, diabetes, cardiovascular disease, delayed initiation of vestibular rehabilitation.