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A case of bilateral parietal cortical laminar necrosis with a loss of vertiginous sensation.

Sugiura Y, Hoshi A, Matsuura Y, Yamamoto T, Ugawa Y

Department of Neurology, School of Medicine Fukushima Medical University, Fukushima, Japan.

Background - Animal experiments demonstrated that there are vestibular cortical areas at the parietal cortex. Moreover, in humans, recent functional neuroimaging studies revealed that caloric stimulation activated the parietoinsular vestibular cortex and optokinetic stimulation activated the parieto-occipital cortex. These activations indicate that the parietal vestibular areas play some role in nystagmus generation or in spatial information processing in the eye movement tasks. Aims of the study - The aim of this communication was to present a patient giving some information about parietal cortical function in nystagmus production and vertigo. Case - We report a 51-year-old, heavy alcoholic man with Bálint syndrome, constructional disability, limb-kinetic apraxia and ideo-motor apraxia. Brain magnetic resonance imaging demonstrated bilateral parietal cortical laminar necrosis anterior to the parieto-occipital sulci without any involvement of the primary sensory and parietoinsular cortices. Optokinetic nystagmus (OKN) was not elicited whereas cold caloric stimulation fully evoked nystagmus toward the opposite side with oscillopsia when eyes opened. However, he did not feel vertiginous sensation when the eyes were closed. Conclusions - These findings suggest that the parietal cortices are indispensable for OKN production and vertiginous sensation.

Published 29 February 2008 in Acta Neurol Scand.
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