Vertigo and dizziness have various causes, ranging from Meniere's disease and vestibular migraine to transient ischemic attacks and stroke (1,2). Up to 40% of patients with vertigo do not receive an explanatory diagnosis in primary healthcare setting and even specialist examination is unable to find out the etiology in some cases (3,4).

Neurovascular compression syndromes (NVC) are caused by abnormal contact (usually a vascular loop) between a vessel and a cranial nerve in the cerebellopontine angle (CPA) (5).Trigeminal neuralgia and hemifacial spasm are the most widely accepted NVC syndromes (5). Glossopharyngeal neuralgia, vestibular paroxysmia and disabling positional vertigo are more controversial entities thought to be caused by NVC (5). 

Contact between the vessel and nerve may be also present in people without any symptoms. It is thought that the susceptibility for symptoms is highest if there is contact at the Root Entry Zone (REZ) (6). REZ for the vestibulocochlear nerve (CN-VIII) extends for about 10 mm from the brainstem (7). 

The purpose of this study was to evaluate whether the course of AICA, type of contact to CN-VIII and vascular contact at REZ might be implicated in patients with vertigo of unexplained etiology.