Vestibular Paroxysmia

Recurrent attacks of vertigo lasting seconds to minutes associated with gait/posture instability, unilateral hypoacusis or tinnitus (occasionally or permanently, triggered by hyperventilation or particular head positions suggest neurovascular cross-compression (NVCC) syndrome of vestibular paroxysmia. The central myelin is formed by oligodendrocytes and peripheral myelin by Schwann cells. The root entry zone of cranial nerves arising from brainstem is composed of transitional myelin and is a vulnerable point. A neurovascular cross-compression (NVCC) is a pathological contact between cranial nerves and vessels. When neurovascular cross-compression occurs on the root entry zone of a cranial nerve which is composed of transitional myelin it results in demyelination of the central (oligodendroglia) myelin. This region varies in length depending on the different cranial nerves and is located close to the brainstem. The vulnerable zone for the eighth cranial nerve (central oligodendrocyte myelin covered) is 6 to 15 mm long and consists of the entire intracranial portion of the nerve. The symptoms are triggered by direct pulsatile compression and/or ephaptic discharges, i.e., pathologically paroxysmal interaxonal transmission between neighboring and in part demyelinated axons. Perhaps there is central hyperactivity in the nucleus, which is induced and maintained by the compression. Carbamazepine in the dose of 600 mg/day or oxcarbazepine in the dose of 900 mg/day decreases the frequency, intensity and duration of attacks.

Neurovascular Cross-Compression of Vestibulocochlear Nerve: Magnetic resonance constructive interference in steady state sequence (CISS) imaging demonstrating a vascular loop causing cross-compression of cisternal segment of the right eighth cranial nerve at two points – one at 2 millimetre & other at 8 millimetre from root entry zone.