Vertical nystagmus in Wernicke’s encephalopathy: pathogenesis and role of central processing of information from the otoliths

Jorge C. Kattah, Collin McClelland, David Samuel Zee

Research output: Contribution to journalArticle

Abstract

Patients with Wernicke’s encephalopathy (WE) often have unusual patterns of vertical nystagmus. Initially there is often a spontaneous upbeating nystagmus that may change to downbeat nystagmus with a change in the direction of gaze, convergence or with vestibular stimuli. Patients also often show a profound loss of the horizontal but not the vertical vestibulo-ocular reflex (VOR). Furthermore, the acute upbeat nystagmus may change to a chronic downbeat nystagmus. We present hypotheses for these features based on (1) the location of vertical gaze-holding networks near the area postrema of the dorsomedial medulla where the blood–brain barrier is located, which we suggest becomes compromised in WE, (2) the location of the vestibular nuclei in the brainstem, medially for the horizontal VOR, and laterally for the vertical VOR, (3) neuronal circuits differ in susceptibility to and in the ability to recover from thiamine deficiency, and (4) impaired processing of otolith information in WE, normally used to modulate translational vestibulo-ocular reflexes, leads to some of the characteristics of the spontaneous vertical nystagmus including the peculiar reversal in its direction with a change in gaze or convergence.

Original languageEnglish (US)
JournalJournal of Neurology
DOIs
StatePublished - Jan 1 2019

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Wernicke Encephalopathy
Pathologic Nystagmus
Vestibulo-Ocular Reflex
Otolithic Membrane
Automatic Data Processing
Thiamine Deficiency
Area Postrema
Vestibular Nuclei
Aptitude
Brain Stem
Direction compound

Keywords

  • Nystagmus
  • Rotation
  • Thiamine deficiency
  • Translation
  • Vestibular

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Cite this

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title = "Vertical nystagmus in Wernicke’s encephalopathy: pathogenesis and role of central processing of information from the otoliths",
abstract = "Patients with Wernicke’s encephalopathy (WE) often have unusual patterns of vertical nystagmus. Initially there is often a spontaneous upbeating nystagmus that may change to downbeat nystagmus with a change in the direction of gaze, convergence or with vestibular stimuli. Patients also often show a profound loss of the horizontal but not the vertical vestibulo-ocular reflex (VOR). Furthermore, the acute upbeat nystagmus may change to a chronic downbeat nystagmus. We present hypotheses for these features based on (1) the location of vertical gaze-holding networks near the area postrema of the dorsomedial medulla where the blood–brain barrier is located, which we suggest becomes compromised in WE, (2) the location of the vestibular nuclei in the brainstem, medially for the horizontal VOR, and laterally for the vertical VOR, (3) neuronal circuits differ in susceptibility to and in the ability to recover from thiamine deficiency, and (4) impaired processing of otolith information in WE, normally used to modulate translational vestibulo-ocular reflexes, leads to some of the characteristics of the spontaneous vertical nystagmus including the peculiar reversal in its direction with a change in gaze or convergence.",
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