![]() ![]() We report transient neurovestibular changes with clinical, serial imaging, and neuropathological findings in a caudal/rostral LMS patient who had sudden cardiorespiratory arrest 3 weeks after his initial stroke that presented with the acute vestibular syndrome (AVS). In general, persistent peripheral vestibular signs in LMS are uncommon and suggest either combined or a medullary/cerebellar stroke with brainstem compression ( 3– 7). HINTS examination battery in LMS is frequently indicative of central localization. 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.įollowing the first clinicopathologic description of a lateral medullary stroke (LMS) ( 1, 2), few clinicopathologic series can be found in the literature, presumably because LMS generally has a favorable outcome. Additionally, truncal lateropulsion was due to combined lateral vestibulospinal tract and lateral reticular nucleus infarction.Ĭonclusion: LMS may rarely be associated with an AVS that either represents or mimics a peripheral vestibulopathy. Although unlikely, the possibility of transient intralabyrinthine arteriolar ischemia cannot be excluded. Neurons and glia within nearby MVN were spared, as predicted by the rapid normalization of the ocular motor signs. Non-ocular motor signs correlated well with structures affected by the infarction. Neuropathological examination showed a left LMS whose extent matched that seen by imaging. 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. Results: The stroke involved the lateral medulla and pontomedullary junction, near the MVN, sparing the cerebellum and pons. Postmortem brainstem analysis was performed. 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. 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. ![]() 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. 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. 5Institute of Anatomy and Cell Biology I, German Center for Vertigo and Balance Disorders, Ludwig-Maximilians-Universität, Munich, Germany.4Department of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.3Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.2Center for Neuropathology and Prion Research, German Center for Vertigo and Balance Disorders, Ludwig-Maximilians-Universität, Munich, Germany.1Department of Neurology, University of Illinois College of Medicine, Peoria, IL, USA. ![]() The most common mechanism of occlusion of the vertebral artery or PICA is atherothrombosis. The majority (80%) of cases are caused by occlusion of the vertebral artery, which gives rise to the PICA and the anterior spinal artery before it joins with the opposite vertebral artery to form the basilar artery. Anatomically the infarcted area in Wallenberg syndrome is supplied by the posterior inferior cerebellar artery (PICA). It turns out occlusion of the PICA accounts for only a small number of cases. The syndrome can also be due to occlusion of the vertebral artery, or the inferior, middle, or superior medullary vessels. The primary pathology of Wallenberg syndrome is occlusion of the posterior inferior cerebellar artery (PICA) or one of its branches (2). Large artery atherothrombotic causes account for about 75% of the cases followed by cardioembolism in 17% and vertebral dissection in 8%(1). There was a predominance of middle aged men. Twenty percent of the ischemic strokes occur in the posterior circulation. If clinicians assume that about half of these suffer from Wallenberg syndrome. Wallenberg syndrome is the most prevalent posterior ischemic stroke syndrome. ![]()
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