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Journal Article

Citation

Wu HY, Wang SJ, Gao ZQ, Jiang H. Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi 2020; 55(8): 754-759.

Copyright

(Copyright © 2020, Zhonghua yi xue hui za zhi she)

DOI

10.3760/cma.j.cn115330-20200616-00504

PMID

32791773

Abstract

OBJECTIVE: To explore the possible pathogenesis of central paroxysmal positional vertigo (CPPV) by analyzing its clinical manifestations and characteristics.

METHODS: The clinical data of 3 patients with CPPV, including 1 male and 2 females, aged 36, 14 and 70 years old respectively, were collected from the Department of Otorhinolaryngology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences from June 2014 to June 2018. The clinical symptoms, nystagmus, other central ocular motor abnormalities, MRI, PET-CT, and laboratory findings were analyzed retrospectively.

RESULTS: All patients showed transient vertigo and nystagmus induced by head changes relative to gravity, but the characteristics of nystagmus did not conform to the typical characteristics of nystagmus in benign paroxysmal positional vertigo. None of patients response to repositioning maneuvers, and all patients presented with the signs of abnormal visual oculomotor system or other symptoms of central system. MRI, PET-CT and blood biochemical tests confirmed that the causes of CPPV in the patients were chronic hemorrhage, inflammation and paraneoplastic cerebellar degeneration. Although the etiology of the three cases is different, the lesion site is involved in the central velocity storage mechanism.

CONCLUSION: The damage of central velocity storage mechanism may lead to the damage of feedback rotation signal correction pathway, and CPPV appears when the head position changes relative to gravity.


Language: zh

Keywords

Benign paroxysmal positional vertigo; Central paroxysmal positional vertigo; Electronystagmography

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