Objective: Horizontal head shaking at 2 to 3 Hz can induce nystagmus in patients with central as well as in patients with peripheral vestibulopathy. However, the characteristics and diagnostic value of this post-head-shaking nystagmus (HSN) have not been studied systematically in central vestibulopathy, and little is known of the mechanisms involved.
Methods: We analyzed spontaneous and HSN and the effects of baclofen, a GABA(B) agonist, in 16 patients with acute lateral medullary infarction.
Results: These patients showed several characteristics of HSN unlike those observed in peripheral vestibulopathy. HSN was observed in 14 of 16 patients (87.5%), and in all cases, the horizontal component beats toward the lesion side, i.e., was ipsilesional. Even in the eight patients with contralesional spontaneous horizontal nystagmus, the HSN was opposite to the spontaneous nystagmus. Three patients showed unusually strong HSN with a maximum slow-phase velocity greater than 60 degrees/second. Visual fixation markedly suppressed HSN and baclofen reduced HSN. In most of the patients, MRI showed infarctions in the caudal or middle portion of the medulla and spared the rostral portion.
Conclusions: We propose that head-shaking nystagmus in lateral medullary infarction is due to unilaterally impaired nodulouvular inhibition of the velocity storage. This proposal is consistent with the results of neuroanatomic studies that demonstrate that Purkinje cells controlling velocity storage in the nodulus and ventral uvula project to the caudal or middle portion of the vestibular nuclei, whereas those subserving visual-vestibular interactions in the flocculus project to the more rostral portion.