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Table of Contents    
LETTER TO EDITOR
Year : 2022  |  Volume : 70  |  Issue : 4  |  Page : 1685-1686

Central Apogeotropic Nystagmus Mimicking A Horizontal Canal “Cupulolithiasis” BPPV


1 Department of Neurology, Division of Neurotology, Aster Medcity, Kochi, Kerala, India
2 Department of Otorhinolaryngology, Division of Neurotology, Aster Medcity, Kochi, Kerala, India

Date of Submission24-Feb-2021
Date of Decision31-Mar-2021
Date of Acceptance05-May-2021
Date of Web Publication30-Aug-2022

Correspondence Address:
Boby Varkey Maramattom
Departments of Neurology, Aster Medcity, Kochi, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0028-3886.355112

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How to cite this article:
Maramattom BV, Sreeram P. Central Apogeotropic Nystagmus Mimicking A Horizontal Canal “Cupulolithiasis” BPPV. Neurol India 2022;70:1685-6

How to cite this URL:
Maramattom BV, Sreeram P. Central Apogeotropic Nystagmus Mimicking A Horizontal Canal “Cupulolithiasis” BPPV. Neurol India [serial online] 2022 [cited 2022 Oct 2];70:1685-6. Available from: https://www.neurologyindia.com/text.asp?2022/70/4/1685/355112




Sir,

Horizontal central positional nystagmus [h-CPN] is uncommon. A 57-year-old man presented with intermittent vertigo and vomiting for 2 days duration. Examination revealed only saccadic pursuit eye movements with a normal Dix-Hallpike test. The McClure Pagnini test elicited a prolonged apogeotropic horizontal nystagmus (AgN) after a brief latency (higher intensity on the right side and lower intensity on the left side) suggestive of a left horizontal canal BPPV (Hc-BPPV) due to cupulolithiasis [Videos 1 and 2]. There were no other cerebellar signs. After repeated Gufoni manoeuvers (forced canalith repositioning manoeuvers × 5) did not ameliorate his vertigo, an MRI brain showed a left cerebellar infarction extending to the nodulus [Figure 1]. MRA showed a left vertebral artery V4 segment occlusion. He was started on antiplatelets, improved in 5 days, and was discharged.
Figure 1: Diffusion-weighted MRI images showing a large left cerebellar PICA territory infarction. The blue arrow shows the infarct extending to the nodulus

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Peripheral Hc-BPPV is of two types. Canalolithiasis produces geotropic nystagmus (GN) on both sides, which is worse toward the affected ear. Contrarily, cupulolithiasis produces apogeotropic nystagmus (AgN) on both sides, that is, less intense on the affected ear. CPN mimicking Hc-BPPV occurs in central vestibular disorders, with impaired central processing of peripheral vestibular signals [Figure 2].
Figure 2: Cartoon [top row]—demonstrating the concordance between the actual and estimated gravitational signals processed by the vestibulocerebellum. Cartoon [bottom row]—demonstrating the discordance between the actual and estimated gravitational signals processed by the vestibulocerebellum. This leads to a “bias” and altered rotational feedback toward the naso-occipital line hat produces apogeotropic nystagmus on either side and may also produce a supine or sitting ipsilesional spontaneous horizontal nystagmus

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A vestibulo-cerebellar pathway (central graviceptive pathway) relays rotational graviceptive information to a feedback center via a velocity storage mechanism (VSM).[1] The VSM is activated by visual and vestibular cues and modified by gravity. It memorizes or stores rotational information. In the normal supine individual, in the ear down position, the estimated gravity feedback correctly points toward the bottom ear (actual and estimated gravity match). In lesions of this pathway, the estimated gravity is wrongly directed (biased) toward or away from the naso-occipital plane resulting in an actual versus estimated gravity mismatch. This is compensated by a corrective rotational cue resulting in sustained horizontal AgN or GN, mimicking the impulses that arrive in the vestibulocerebellum in Hc-BPPV.[2]

In conclusion, our patient had AgN suggesting a left HC BPPV, which was in fact due to a left large cerebellar infarct involving the nodulus. He had very subtle central signs and the cerebellar infarct could have been missed without imaging. AgN should definitely alert the clinician to the possibility of a CPN. Central lesions should also be considered in the differential diagnosis of pure AgN or GN especially when the nystagmus is persistent (i.e., lasts >1 min), lacks fatigability, or is unresponsive to repeated canalith repositioning manoeuvers.[3]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial Support and Sponsorship

Nil.

Conflicts of Interest

There are no conflicts of interest.



 
  References Top

1.
Laurens J, Angelaki DE. The functional significance of velocity storage and its dependence on gravity. Exp Brain Res 2011;210:407-22.  Back to cited text no. 1
    
2.
Choi J, Glasauer S, Kim JH, Zee DS, Kim J, Characteristics and mechanism of apogeotropic central positional nystagmus. Brain 2018;141:762-75.  Back to cited text no. 2
    
3.
Bertholon P, Tringali S, Faye MB, Antoine JC, Martin C. Prospective study of positional nystagmus in 100 consecutive patients. Ann Otol Rhinol Laryngol 2006;115:587-94.  Back to cited text no. 3
    


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