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Transient Vestibulopathy in Wallenberg’s Syndrome: Pathologic Analysis
OBJECTIVE: To report an unusual lateral medullary stroke (LMS) associated with transient unidirectional horizontal, nystagmus, and decreased horizontal vestibulo–ocular reflex (h-VOR) gain that mimicked a peripheral vestibulopathy. MRI suggested involvement of caudal medial vestibular nucleus (MVN);...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5434105/ https://www.ncbi.nlm.nih.gov/pubmed/28567027 http://dx.doi.org/10.3389/fneur.2017.00191 |
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author | Kattah, Jorge C. Saber Tehrani, Ali S. Roeber, Sigrun Gujrati, Meena Bach, Sarah E. Newman Toker, David E. Blitz, Ari M. Horn, Anja K. E. |
author_facet | Kattah, Jorge C. Saber Tehrani, Ali S. Roeber, Sigrun Gujrati, Meena Bach, Sarah E. Newman Toker, David E. Blitz, Ari M. Horn, Anja K. E. |
author_sort | Kattah, Jorge C. |
collection | PubMed |
description | OBJECTIVE: To report an unusual lateral medullary stroke (LMS) associated with transient unidirectional horizontal, nystagmus, and decreased horizontal vestibulo–ocular reflex (h-VOR) gain that mimicked a peripheral vestibulopathy. MRI suggested involvement of caudal medial vestibular nucleus (MVN); however, the rapid resolution of the nystagmus and improved h-VOR gain favored transient ischemia without infarction. Decreased h-VOR gain is expected with peripheral vestibular lesions within the labyrinth or superior vestibular nerve; less frequently lateral pontine strokes involving the vestibular root entry, the vestibular fascicle, or neurons within the MVN may be responsible. The h-VOR is typically normal in LMS. METHODS: Clinicopathologic examination of a 61-year-old man with an acute vestibular syndrome (AVS) and left LMS who died 3 weeks after the stroke. Postmortem brainstem analysis was performed. RESULTS: The stroke involved the lateral medulla and pontomedullary junction, near the MVN, sparing the cerebellum and pons. To explain transient vestibular findings there are two possible hypotheses; the first would be that the MVN survived the ischemic process and would be histologically intact, and the second that vestibular afferents in the horizontal semicircular canal were ischemic and recovered after the ischemic process. Neuropathological examination showed a left LMS whose extent matched that seen by imaging. Non-ocular motor signs correlated well with structures affected by the infarction. Neurons and glia within nearby MVN were spared, as predicted by the rapid normalization of the ocular motor signs. Although unlikely, the possibility of transient intralabyrinthine arteriolar ischemia cannot be excluded. Additionally, truncal lateropulsion was due to combined lateral vestibulospinal tract and lateral reticular nucleus infarction. CONCLUSION: LMS may rarely be associated with an AVS that either represents or mimics a peripheral vestibulopathy. To our knowledge, this is the first neuropathologic examination of the brainstem of an LMS associated with transient vestibular findings occurring in the context of an anterior/posterior (AICA/PICA) cerebellar arterial variant stroke. |
format | Online Article Text |
id | pubmed-5434105 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-54341052017-05-31 Transient Vestibulopathy in Wallenberg’s Syndrome: Pathologic Analysis Kattah, Jorge C. Saber Tehrani, Ali S. Roeber, Sigrun Gujrati, Meena Bach, Sarah E. Newman Toker, David E. Blitz, Ari M. Horn, Anja K. E. Front Neurol Neuroscience OBJECTIVE: To report an unusual lateral medullary stroke (LMS) associated with transient unidirectional horizontal, nystagmus, and decreased horizontal vestibulo–ocular reflex (h-VOR) gain that mimicked a peripheral vestibulopathy. MRI suggested involvement of caudal medial vestibular nucleus (MVN); however, the rapid resolution of the nystagmus and improved h-VOR gain favored transient ischemia without infarction. Decreased h-VOR gain is expected with peripheral vestibular lesions within the labyrinth or superior vestibular nerve; less frequently lateral pontine strokes involving the vestibular root entry, the vestibular fascicle, or neurons within the MVN may be responsible. The h-VOR is typically normal in LMS. METHODS: Clinicopathologic examination of a 61-year-old man with an acute vestibular syndrome (AVS) and left LMS who died 3 weeks after the stroke. Postmortem brainstem analysis was performed. RESULTS: The stroke involved the lateral medulla and pontomedullary junction, near the MVN, sparing the cerebellum and pons. To explain transient vestibular findings there are two possible hypotheses; the first would be that the MVN survived the ischemic process and would be histologically intact, and the second that vestibular afferents in the horizontal semicircular canal were ischemic and recovered after the ischemic process. Neuropathological examination showed a left LMS whose extent matched that seen by imaging. Non-ocular motor signs correlated well with structures affected by the infarction. Neurons and glia within nearby MVN were spared, as predicted by the rapid normalization of the ocular motor signs. Although unlikely, the possibility of transient intralabyrinthine arteriolar ischemia cannot be excluded. Additionally, truncal lateropulsion was due to combined lateral vestibulospinal tract and lateral reticular nucleus infarction. CONCLUSION: LMS may rarely be associated with an AVS that either represents or mimics a peripheral vestibulopathy. To our knowledge, this is the first neuropathologic examination of the brainstem of an LMS associated with transient vestibular findings occurring in the context of an anterior/posterior (AICA/PICA) cerebellar arterial variant stroke. Frontiers Media S.A. 2017-05-17 /pmc/articles/PMC5434105/ /pubmed/28567027 http://dx.doi.org/10.3389/fneur.2017.00191 Text en Copyright © 2017 Kattah, Saber Tehrani, Roeber, Gujrati, Bach, Newman Toker, Blitz and Horn. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Kattah, Jorge C. Saber Tehrani, Ali S. Roeber, Sigrun Gujrati, Meena Bach, Sarah E. Newman Toker, David E. Blitz, Ari M. Horn, Anja K. E. Transient Vestibulopathy in Wallenberg’s Syndrome: Pathologic Analysis |
title | Transient Vestibulopathy in Wallenberg’s Syndrome: Pathologic Analysis |
title_full | Transient Vestibulopathy in Wallenberg’s Syndrome: Pathologic Analysis |
title_fullStr | Transient Vestibulopathy in Wallenberg’s Syndrome: Pathologic Analysis |
title_full_unstemmed | Transient Vestibulopathy in Wallenberg’s Syndrome: Pathologic Analysis |
title_short | Transient Vestibulopathy in Wallenberg’s Syndrome: Pathologic Analysis |
title_sort | transient vestibulopathy in wallenberg’s syndrome: pathologic analysis |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5434105/ https://www.ncbi.nlm.nih.gov/pubmed/28567027 http://dx.doi.org/10.3389/fneur.2017.00191 |
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