Head-shaking nystagmus in lateral medullary infarction - Patterns and possible mechanisms

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 GABAB 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. ©2007AAN Enterprises, Inc.; Indications:6 patients with horizontal head shaking nystagmus [maximum slow-phase velocity (SPV) >20 degrees/second; 4 chronic (more than 2 months) and 2 subacute (9 and 21 days)]. Coexisting disease: lateral medullary infarction.; Patients:6 male and female patients, age range 39-69 years (mean age 55.6 years). Follow up: 1 month.; TypeofStudy:An open study investigating the effect of Lioresal, a gamma aminobutyric acid B receptor (GABA B) agonist on head-shaking nystagmus (HSN) in patients with lateral medullary infarction to determine the possible involvement of the nodulouvular inhibitory pathways on the velocity storage in the generation of HSN.; DosageDuration:30 mg daily for 1 week.; Results:Lioresal significantly reduced the median SPV of the first 3 beats of horizontal HSN from 32 degrees/ second before treatment to 12 degrees/second after 1 week of treatment. The maximum SPV reduced by >40% in all 6 patients, and by >70% (mean decrement: 60.6%) in 2 patients. 1 month after discontinuing Lioresal, maximum SPV increased back to 26 degrees/second.; AdverseEffects:No adverse events were mentioned.; AuthorsConclusions:The suppression of HSN by baclofen observed in our patients strongly supports our proposition that asymmetric velocity storage due to unilateral damage of nodulouvular inhibition on the velocity storage by lateral medullary lesions generates ipsilesional HSN.; FreeText:HSN was recorded by 3-dimensional video-oculography (VOG) before and after Lioresal treatment and at 1 month after Lioresal discontinuation. SPV of the first 3 beats of HSN was measured.