Effect of Ibudilast on the Reciprocal Inhibitory Visual–Vestibular Interaction Closely Related to Dizziness after Cerebral Ischemia

Inoue, Nobuhiro; Fukuda, Shingo; Inada, Tetsuya; Sameshima, Eiichi; Tokushima, Yoko; Harada, Mikio

doi:10.1016/j.jstrokecerebrovasdis.2012.09.007

Cited by 7 publications

(5 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…By using the standard xenon-enhanced CT CBF system, we have carried out CBF measurements in multiple brain regions of post-stroke patients. As we documented elsewhere [15][16][17], the ischemic lesions in our study population were located in infra-and supratentorial areas and not only in the VISC and PIVC, indicating that ischemia in other brain areas may elicit dizziness. From 2 to 6 months after the start of ibudilast therapy, all eleven [16] and nine [17] patients resolved their dizziness respectively.…”

Section: Evidence For a Decreased Cbf In The Vestibular-visual Corticsupporting

confidence: 72%

“…We next examined the therapeutic effects of ibudilast, which is reportedly known to increase the CBF by facilitating the vasomotor reactivity of cerebral vasculature [16,17], in patients with dizziness. In patients treated with ibudilast, the amelioration of dizziness was accompanied by a signi icant increase in the CBF in only the VISC, bar graph [6] in igure E. To con irm the presence of an inhibitory effect from the PIVC to the VISC, we recorded the CBF after ACZ loading.…”

Section: Evidence For a Decreased Cbf In The Vestibular-visual Corticmentioning

confidence: 99%

See 1 more Smart Citation

Post-stroke dizziness of visual-vestibular cortices origin

Inoue¹,

Goto²

2020

J Neurosci Neurol Disord

View full text Add to dashboard Cite

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.

show abstract

Section: Evidence For a Decreased Cbf In The Vestibular-visual Corticsupporting

confidence: 72%

Section: Evidence For a Decreased Cbf In The Vestibular-visual Corticmentioning

confidence: 99%

Post-stroke dizziness of visual-vestibular cortices origin

Inoue¹,

Goto²

2020

J Neurosci Neurol Disord

View full text Add to dashboard Cite

show abstract

“…Over the last two decades multiple human neuroimaging studies have reported a reciprocal interaction between the vestibular and the visual cortex (Brandt et al 1998(Brandt et al , 2002Deutschländer et al 2002;Dieterich et al 2003;Della-Justina et al 2014). Although some of the studies should be interpreted with caution since the sample sizes were small (Brandt et al 1998;Bense et al 2001;Inoue et al 2014) and results were not always corrected properly for multiple testing (Deutschländer et al 2002), the finding of a visual-vestibular interaction seems robust. Notably, a recent study on multisensory interaction using near infrared caloric vestibular stimulation failed to find a reciprocal visual-vestibular interaction (Ferrè et al 2015).…”

Section: Introductionmentioning

confidence: 99%

The role of delta and theta oscillations during ego-motion in healthy adult volunteers

et al. 2021

View full text Add to dashboard Cite

The successful cortical processing of multisensory input typically requires the integration of data represented in different reference systems to perform many fundamental tasks, such as bipedal locomotion. Animal studies have provided insights into the integration processes performed by the neocortex and have identified region specific tuning curves for different reference frames during ego-motion. Yet, there remains almost no data on this topic in humans.In this study, an experiment originally performed in animal research with the aim to identify brain regions modulated by the position of the head and eyes relative to a translational ego-motion was adapted for humans. Subjects sitting on a motion platform were accelerated along a translational pathway with either eyes and head aligned or a 20° yaw-plane offset relative to the motion direction while EEG was recorded.Using a distributed source localization approach, it was found that activity in area PFm, a part of Brodmann area 40, was modulated by the congruency of translational motion direction, eye, and head position. In addition, an asymmetry between the hemispheres in the opercular-insular region was observed during the cortical processing of the vestibular input. A frequency specific analysis revealed that low-frequency oscillations in the delta- and theta-band are modulated by vestibular stimulation. Source-localization estimated that the observed low-frequency oscillations are generated by vestibular core-regions, such as the parieto-opercular region and frontal areas like the mid-orbital gyrus and the medial frontal gyrus.

show abstract

“…Ibudilast (3-isobutyryl-2-isopropylpyrazolo-[1, 5-a] pyridine) is a neuroimmune modulator and phosphodiesterase inhibitor that demonstrates neuroprotective, anti-inflammatory actions via glial cell inhibition [ 46 , 47 , 48 ] and antagonism of toll-like receptor 4 [ 49 ]. Ibudilast has long been used to treat patients with cerebrovascular disorders and has been found to be neuroprotective following ischemia due to its anti-inflammatory properties and anti-aggregatory actions on platelets [ 36 , 46 , 50 , 51 , 52 , 53 , 54 ].…”

Section: Methodsmentioning

confidence: 99%

Neuroimmune Support of Neuronal Regeneration and Neuroplasticity following Cerebral Ischemia in Juvenile Mice

Marquez-Ortiz,

Tesic,

Hernandez

et al. 2023

Brain Sciences

View full text Add to dashboard Cite

Ischemic damage to the brain and loss of neurons contribute to functional disabilities in many stroke survivors. Recovery of neuroplasticity is critical to restoration of function and improved quality of life. Stroke and neurological deficits occur in both adults and children, and yet it is well documented that the developing brain has remarkable plasticity which promotes increased post-ischemic functional recovery compared with adults. However, the mechanisms underlying post-stroke recovery in the young brain have not been fully explored. We observed opposing responses to experimental cerebral ischemia in juvenile and adult mice, with substantial neural regeneration and enhanced neuroplasticity detected in the juvenile brain that was not found in adults. We demonstrate strikingly different stroke-induced neuroimmune responses that are deleterious in adults and protective in juveniles, supporting neural regeneration and plasticity. Understanding age-related differences in neuronal repair and regeneration, restoration of neural network function, and neuroimmune signaling in the stroke-injured brain may offer new insights for the development of novel therapeutic strategies for stroke rehabilitation.

show abstract

Effect of Ibudilast on the Reciprocal Inhibitory Visual–Vestibular Interaction Closely Related to Dizziness after Cerebral Ischemia

Cited by 7 publications

References 21 publications

Post-stroke dizziness of visual-vestibular cortices origin

Post-stroke dizziness of visual-vestibular cortices origin

The role of delta and theta oscillations during ego-motion in healthy adult volunteers

Neuroimmune Support of Neuronal Regeneration and Neuroplasticity following Cerebral Ischemia in Juvenile Mice

Contact Info

Product

Resources

About