Eyes wide shut: Horizontal direction changing nystagmus in a left cerebellar-medullary stroke. Favourable outcome after thrombolysis.

J Stroke Cerebrovasc Dis

Institute of Neurology, Department of Neurosciences, Presidio Ospedaliero "Pugliese", AOU "Renato Dulbecco", Catanzaro 88100, Italy. Electronic address:

Published: November 2024

AI Article Synopsis

  • A 78-year-old man experienced an acute stroke due to a posterior inferior cerebellar artery blockage, resulting in severe vertigo, gait imbalance, and dysphagia.
  • Clinical examination revealed complex nystagmus patterns: a right-beating nystagmus in primary gaze and a left-beating nystagmus when looking left, indicating central nervous system involvement.
  • Brain imaging confirmed an acute stroke affecting the left medulla and cerebellum, suggesting that damage to specific brain structures can lead to diverse nystagmus presentations associated with central lesions.

Article Abstract

Objective: To describe a patient with a posterior inferior cerebellar artery stroke exhibiting a horizontal direction changing nystagmus with a complex clinical phenotype.

Materials And Methods: A 78-year-old man presented with acute vertigo and gait imbalance. He was dysphagic and ataxic on the left side. He had a fast, small-amplitude right-beating nystagmus in the primary gaze position and in the gaze towards the right. Towards the left, a coarse left-beating nystagmus was seen.

Results: Radiographic leftwards ocular deviation was evident on admission CT. Intravenous fibrinolysis was administered. 48-hour Holter-EKG, transthoracic ecochardiogram, and transcranial doppler were unremarkable. Brain MRI demonstrated an acute stroke involving the left medulla and cerebellum, mainly within the territory of the ipsilateral posterior inferior cerebellar artery.

Discussion And Conclusions: Horizontal direction changing nystagmus can arise secondary to central lesions as brainstem strokes, it can be spontaneous or gaze-evoked and characteristically remains unchanged after fixation removal. In our case, the vestibular spontaneous and contralesional nystagmus was likely related to lower-brainstem damage; on the other hand, the ipsilesional gaze-evoked nystagmus might be related to lesions of the nucleus prepositus hypoglossi and/or cerebellum, both playing an important role in gaze-holding. Our findings suggest that central lesions with concurrent involvement of the ipsilateral vestibulo-ocular and horizontal gaze-holding pathways can cause direction changing nystagmus with complex phenotypes.

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http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2024.107986DOI Listing

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