Vestibular Paroxysmia


In this condition, the patient suffers from short spells of vertigo which occur recurrently. It is due to compression of the vestibular or balance nerve.


Compression or damage to the vestibular nerve may occur in varying situations like compression by blood vessels, which is the commonest cause. The vessel implicated is usually a branch of the anterior inferior cerebellar artery (AICA). The attacks are brought on by the pulsating artery compressing the nerve leading to nerve conduction block. Other less common causes include post-radiation or post-surgery fibrosis, vestibular neuritis, tumors like vestibular schwannoma, etc.


Vestibular paroxysmia is suspected if the clinical picture has the following characteristics:
  • Short spells of vertigo lasting seconds to minutes.
  • Instability
  • Spells may be triggered by change of head position
  • Hyperventilation may trigger an attack
  • Hearing problem or ringing in the ear may occur during the episode which decreases once the episode is over


The following investigations should be done
  • Audiometry: The patient may have fluctuating hearing loss or normal hearing
  • Videonystagmography (VNG): Nystagmus may be detected on hyperventilation and head shaking tests. In some patients, positional tests may also elicit nystagmus but this nystagmus will be different from the nystagmus of BPPV.
  • EEG to rule out seizures, which may mimic vestibular paroxysmia symptoms.
  • MRI brain with gadolinium enhancement: 3D constructive interference in steady state and CISS should be done. This imaging will be the final proof of microvascular compression.


This condition is considered to be analogous to trigeminal neuralgia. The first line of treatment includes sodium channel blockers like Carbamazepine and Oxcarbamazepine. These drugs are used as a therapeutic trial initially to confirm the presence of microvascular compression. Symptomatic relief by these medicines practically confirms the diagnosis. The recommended dose is Carbamazepine – 200-600mg/day and Oxcarbamazepine – 300-900mg/day. Treatment usually begins with Carbamazepine 100 mg BD and is increase to provide optimum relief. Vestibular sedatives are not effective in these patients.

In patients who are not optimally controlled with these drugs and present with intractable symptoms, surgery in the form of Microvascular Decompression may be done. This surgery is done endoscopically. The VII-VIII nerve complex is identified and the vascular loop is either cauterized or a sponge is placed between the blood vessel and nerve to prevent compression.

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