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Head-shaking nystagmus in lateral medullary infarction: patterns and possible mechanisms.
Neurology. 2007 Apr 24; 68(17):1337-44.Neur

Abstract

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.

Authors+Show Affiliations

Department of Neurology, College of Medicine, Seoul National University, Seoul National University Bundang Hospital, Seoul, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17452577

Citation

Choi, K-D, et al. "Head-shaking Nystagmus in Lateral Medullary Infarction: Patterns and Possible Mechanisms." Neurology, vol. 68, no. 17, 2007, pp. 1337-44.
Choi KD, Oh SY, Park SH, et al. Head-shaking nystagmus in lateral medullary infarction: patterns and possible mechanisms. Neurology. 2007;68(17):1337-44.
Choi, K. D., Oh, S. Y., Park, S. H., Kim, J. H., Koo, J. W., & Kim, J. S. (2007). Head-shaking nystagmus in lateral medullary infarction: patterns and possible mechanisms. Neurology, 68(17), 1337-44.
Choi KD, et al. Head-shaking Nystagmus in Lateral Medullary Infarction: Patterns and Possible Mechanisms. Neurology. 2007 Apr 24;68(17):1337-44. PubMed PMID: 17452577.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Head-shaking nystagmus in lateral medullary infarction: patterns and possible mechanisms. AU - Choi,K-D, AU - Oh,S-Y, AU - Park,S-H, AU - Kim,J-H, AU - Koo,J-W, AU - Kim,J S, PY - 2007/4/25/pubmed PY - 2007/5/11/medline PY - 2007/4/25/entrez SP - 1337 EP - 44 JF - Neurology JO - Neurology VL - 68 IS - 17 N2 - 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. SN - 1526-632X UR - https://www.unboundmedicine.com/medline/citation/17452577/Head_shaking_nystagmus_in_lateral_medullary_infarction:_patterns_and_possible_mechanisms_ L2 - http://www.neurology.org/cgi/pmidlookup?view=long&pmid=17452577 DB - PRIME DP - Unbound Medicine ER -