Marianne Dieterich1, Thomas Brandt2. 1. From the Department of Neurology (M.D.), German Center for Vertigo and Balance Disorders (M.D., T.B.), Clinical Neuroscience (T.B.), Ludwig-Maximilians University, Munich; and Munich Cluster for Systems Neurology (SyNergy) (M.D.), Munich, Germany. marianne.dieterich@med.uni-muenchen.de. 2. From the Department of Neurology (M.D.), German Center for Vertigo and Balance Disorders (M.D., T.B.), Clinical Neuroscience (T.B.), Ludwig-Maximilians University, Munich; and Munich Cluster for Systems Neurology (SyNergy) (M.D.), Munich, Germany.
Abstract
OBJECTIVES: The aim of the current study was, first, to determine the critical causative vestibular areas that in exceptional cases manifest with transient vertigo or dizziness in acute strokes of the middle cerebral artery, and second, to try to explain why in most cases unilateral lesions of these areas manifest without vertigo. METHODS: We determined the ischemic areas of the 10 published cases by overlapping the CT/MRI lesions and attributed them to the temporoparietal vestibular network. RESULTS: These overlap areas were located either in the posterior retroinsular cortex (n = 8), i.e., the parieto-insular vestibular cortex, or the separate parietal vestibular cortex (n = 2). CONCLUSION: Thus, rare vestibular cortical vertigo is mostly elicited by acute lesions of the core region of the retroinsular vestibular network. However, the more interesting question is related to the lack of cortical vertigo when this area is affected. We propose a concept to explain how the unaffected opposite hemisphere can suppress vertigo. This is based on visual-vestibular interaction for motion perception and orientation. It is the hemisphere in which vestibular and visual inputs are in agreement, which is the more reliable and determines the global perception of body orientation and motion.
OBJECTIVES: The aim of the current study was, first, to determine the critical causative vestibular areas that in exceptional cases manifest with transient vertigo or dizziness in acute strokes of the middle cerebral artery, and second, to try to explain why in most cases unilateral lesions of these areas manifest without vertigo. METHODS: We determined the ischemic areas of the 10 published cases by overlapping the CT/MRI lesions and attributed them to the temporoparietal vestibular network. RESULTS: These overlap areas were located either in the posterior retroinsular cortex (n = 8), i.e., the parieto-insular vestibular cortex, or the separate parietal vestibular cortex (n = 2). CONCLUSION: Thus, rare vestibular cortical vertigo is mostly elicited by acute lesions of the core region of the retroinsular vestibular network. However, the more interesting question is related to the lack of cortical vertigo when this area is affected. We propose a concept to explain how the unaffected opposite hemisphere can suppress vertigo. This is based on visual-vestibular interaction for motion perception and orientation. It is the hemisphere in which vestibular and visual inputs are in agreement, which is the more reliable and determines the global perception of body orientation and motion.