Abstract

Backgrund and Objective: To characterize clinical features of the rotational vertebral artery syndrome. The syndrome of rotational vertebral artery occlusion is characterized by recurrent attacks of vertigo, nystagmus, and ataxia, which have been ascribed to compression of the dominant vertebral artery, usually at the atlantoaxial joint, which is usually induced by head turning toward the contralateral side. Materials and Methods: Of the patients who had been evaluated in the Neurotology/Neuro-ophthalmology Clinic of Seoul National University Bundang Hospital from June, 2003 to October, 2004, four patients with a diagnosis of the rotational vertebral artery syndrome were included. All the Patients received full bedside neurotolgical evaluation by one of the author, which included the tests for spontaneous, gaze-evoked, vibration-induced, head shaking, and positioning/positional nystagmus, and head thrust test in addition to routine neurological examination. For positional/positioning nystagmus, patients bent down, straightened up, and turned their head to either side while sitting. And the patients were moved from sitting to lying down on their back. Subsequently, the head was turned to either side while lying down. The patient also underwent both Hallpikes and straight head hanging test. Each position was maintained at least for 30s. The nystagmus was observed on the video monitor by using video goggles with or without visual fixation. Eye movements were also measured by using three dimensional video-oculography (SMI, Germany).
Results
Of the four patients, three showed vertical nystagmus several seconds after head rotation toward one side while either sitting or lying down. The other patient developed mixed horizontal, torsional, and vertical nystagmus with the horizontal component beating toward the side of the compressed vertebral artery. Two patients showed reversal of the nystagmus even though the rotated head posture was maintained. While the vertigo and nystagmus were induced during both sitting and lying down in three patients, those developed only during sitting in one patient. In two patients, transient tinnitus accompanied the vertigo. In all patients, the vertebral artery was hypoplastic in one side. In three patients with symptoms while lying down, dynamic angiography documented compression or occlusion of the vertebral artery at the atlantoaxial junction.
Conclusion
In view of the different patterns of nystagmus, various mechanisms may be involved in the generation of symptoms in rotational vertebral artery syndrome. This syndrome may result from excitation or suppression of the vestibular structures in the lower brainstem, caudal cerebellum, or peripheral labyrinth. This syndrome should be considered as a differential diagnosis in patients with positional vertigo, especially while sitting or standing.