Abstract

Many patients with chronic cerebrovascular diseases complain “dizziness”, which is a distortion of static gravitational orientation, or an erroneous perception of motion of the sufferer or of the environment. In the vestibular cortical system, the parieto-insular vestibular cortex (PIVC) serves as the core region having the strong interconnections with other vestibular cortical areas and the vestibular brainstem nuclei. By forming the reciprocal inhibitory interactions with the visual cortex (VISC), it also plays a pivotal role in a multisensory mechanism for self-motion perception. In a line of our studies on post-stroke patients, we found that there was a significant decrease in the cerebral blood flow in both the VISC and PIVC in the patients who suffered from dizziness. In this article, we provide a new concept that due to dysfunction of the visual-vestibular interaction loop, low cerebral blood perfusion in the PIVC and VISC might elicit post-stroke dizziness.

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