2014
DOI: 10.3342/ceo.2014.7.2.138
|View full text |Cite
|
Sign up to set email alerts
|

Persistent Direction-Fixed Nystagmus Following Canalith Repositioning Maneuver for Horizontal Canal BPPV: A Case of Canalith Jam

Abstract: The authors report a 64-year-old man who developed persistent direction fixed nystagmus after a canalith repositioning maneuver for horizontal canal benign paroxysmal positional vertigo (HC-BPPV). The patient was initially diagnosed with right HC-BPPV given that the Dix-Hallpike test showed geotropic horizontal nystagmus that was more pronounced on the right side, although the roll test did not show any positional nystagmus. The patient was treated with a canalith repositioning maneuver (Lempert maneuver). The… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2

Citation Types

0
15
0
1

Year Published

2016
2016
2023
2023

Publication Types

Select...
10

Relationship

0
10

Authors

Journals

citations
Cited by 18 publications
(16 citation statements)
references
References 7 publications
0
15
0
1
Order By: Relevance
“…As already described for HSC-canalith jam ( 87 , 88 ), this mechanism may prevent both high- and low-frequency responses for the SC affected (namely head impulses and otoconial shifts, respectively) by blocking endolymphatic flows, likewise surgical plugging ( 89 ), thus explaining severe impairment of canal VOR-gain. Though canalith jam has been described for HSC in several reports, occurring either spontaneously ( 87 , 88 , 90 , 91 ) or as a result of inappropriate CRP ( 92 94 ), a similar condition involving PSC has been recently implied as the hypothetical pathomechanism for spontaneous DBN receding after proper physical treatment ( 95 ). Whereas, spontaneous nystagmus resulting from HSC-canalith jam overlaps presenting signs of acute vestibular loss, spontaneous VOG findings due to a PSC involvement should be mainly torsional/vertical aligning with vertical SC axis, thus mimicking CNS pathologies.…”
Section: Discussionmentioning
confidence: 99%
“…As already described for HSC-canalith jam ( 87 , 88 ), this mechanism may prevent both high- and low-frequency responses for the SC affected (namely head impulses and otoconial shifts, respectively) by blocking endolymphatic flows, likewise surgical plugging ( 89 ), thus explaining severe impairment of canal VOR-gain. Though canalith jam has been described for HSC in several reports, occurring either spontaneously ( 87 , 88 , 90 , 91 ) or as a result of inappropriate CRP ( 92 94 ), a similar condition involving PSC has been recently implied as the hypothetical pathomechanism for spontaneous DBN receding after proper physical treatment ( 95 ). Whereas, spontaneous nystagmus resulting from HSC-canalith jam overlaps presenting signs of acute vestibular loss, spontaneous VOG findings due to a PSC involvement should be mainly torsional/vertical aligning with vertical SC axis, thus mimicking CNS pathologies.…”
Section: Discussionmentioning
confidence: 99%
“…There are no other side effects except dizziness and symptoms of the vegetative nervous system. Persistent nystagmus has occasionally been reported after restoration, but it can be rapidly alleviated [7]. Brandt-Daroff exercise method and repeated CRM are recommended for the cases of CRM failure; while drug therapy is only auxiliary [8] and they all have no impact on the recurrence rate [9].…”
Section: Introductionmentioning
confidence: 99%
“…There are some cases that lesion side determined by vestibular function tests is not identical between the tests at different time points. Besides the central nystagmus [2-4] and atypical benign paroxysmal positional vertigo [5,6], most probable explanation for this is recovery spontaneous nystagmus (rSN). rSN usually follows the initial paralytic nystagmus [7].…”
Section: Introductionmentioning
confidence: 99%