Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2012
Effect of ibudilast on the reciprocal inhibitory visual-vestibular interaction closely related to dizziness after cerebral ischemia.
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Inoue Nobuhiro, Fukuda Shingo, Inada Tetsuya, Sameshima Eiichi, Tokushima Yoko, Harada Mikio
Аннотация
BACKGROUND: Many patients with chronic cerebrovascular diseases suffer dizziness. Our earlier findings suggested that prolonged terms of dizziness episodes may decrease the regional cerebral blood flow (CBF) in the occipital visual cortex via a remote effect from the vestibular cortex.
METHODS: We studied 9 patients who suffered episodes of dizziness since the onset of chronic cerebral ischemia. Their at-rest CBF was measured at entry into the study and approximately 3 months after the start of ibudilast therapy when all patients reported the resolution of dizziness.
RESULTS: After 3 months of ibudilast their at-rest CBF was significantly increased in the left occipital lobe (P = .02). CBF after acetazolamide (ACZ) loading was significantly increased in the bilateral occipital lobes (right, P = .049; left, P = .02) and in the bilateral parieto-insular vestibular cortex (PIVC; right and left, P = .02). There were no significant CBF changes in any other areas.
CONCLUSIONS: Our findings indicate that the occipital cortex and PIVC were implicated in their dizziness after cerebral ischemia. We discuss the underlying mechanism(s) and the relationship between dizziness and reciprocal inhibitory visual-vestibular interactions.
METHODS: We studied 9 patients who suffered episodes of dizziness since the onset of chronic cerebral ischemia. Their at-rest CBF was measured at entry into the study and approximately 3 months after the start of ibudilast therapy when all patients reported the resolution of dizziness.
RESULTS: After 3 months of ibudilast their at-rest CBF was significantly increased in the left occipital lobe (P = .02). CBF after acetazolamide (ACZ) loading was significantly increased in the bilateral occipital lobes (right, P = .049; left, P = .02) and in the bilateral parieto-insular vestibular cortex (PIVC; right and left, P = .02). There were no significant CBF changes in any other areas.
CONCLUSIONS: Our findings indicate that the occipital cortex and PIVC were implicated in their dizziness after cerebral ischemia. We discuss the underlying mechanism(s) and the relationship between dizziness and reciprocal inhibitory visual-vestibular interactions.