Abstract

Background
and Objectives: To clarify the mechanism of head-shaking nystagmus (HSN) in lateral medullary infarctions. It has been known that HSN is generated by the combination of asymmetric vestibular inputs due to Ewald's second law and central velocity-storage mechanism. However, the mechanism and lateralizing value of HSN in central vestibular lesions remains to be elucidated. Materials and Method: HSN was observed with video-Frenzel goggles and recorded with three dimensional video-oculography (SMI, Teltow, Germany) in three patients with lateral medullary infarction. HSN was induced by passive head oscillations in the yaw plane at 2 to 3 Hz. Tilt suppression of the post-rotatory nystagmus was evaluated by bending forward after step velocity rotation (acceleration, 100°/s2; velocity, 100°/s) of the patients to either side around a vertical axis.
Results
All the patients showed contralesionally beating spontaneous nystagmus with torsional and upbeat components during the acute phase. However, horizontal head oscillations immediately reversed the directions of the nystagmus which was suppressed by visual fixation. In one patient, HSN was not suppressed by tilting of the head. The other two patients showed rapid habituation of HSN, which did not permit evaluating the effect of head tilt on HSN. Rotation test disclosed asymmetric vestibulo-ocular reflex (VOR) with lower gain and time constant in rotation to the lesion side. The visual augmentation and suppression of the VOR were normal. While head tilt suppressed the post-rotatory nystagmus after rotation to the sound side, no suppression occurred after rotation to the lesion side,
Conclusion
The ipsilesionally beating HSN in lateral medullary infarction may be explained by unilateral damage to the inhibitory nodulo-vestibular projections, which control the velocity-storage mechanism. The reversal of spontaneous nystagmus by head oscillation may be a characteristic sign of central vestibular disorder.