scholarly journals Post-stroke dizziness of visual-vestibular cortices origin

2020 ◽  
Vol 4 (2) ◽  
pp. 075-078
Author(s):  
Inoue Nobuhiro ◽  
Goto Satoshi

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.

2018 ◽  
Vol 120 (3) ◽  
pp. 1438-1450 ◽  
Author(s):  
Sebastian M. Frank ◽  
Mark W. Greenlee

Here, we review the structure and function of a core region in the vestibular cortex of humans that is located in the midposterior Sylvian fissure and referred to as the parieto-insular vestibular cortex (PIVC). Previous studies have investigated PIVC by using vestibular or visual motion stimuli and have observed activations that were distributed across multiple anatomical structures, including the temporo-parietal junction, retroinsula, parietal operculum, and posterior insula. However, it has remained unclear whether all of these anatomical areas correspond to PIVC and whether PIVC responds to both vestibular and visual stimuli. Recent results suggest that the region that has been referred to as PIVC in previous studies consists of multiple areas with different anatomical correlates and different functional specializations. Specifically, a vestibular but not visual area is located in the parietal operculum, close to the posterior insula, and likely corresponds to the nonhuman primate PIVC, while a visual-vestibular area is located in the retroinsular cortex and is referred to, for historical reasons, as the posterior insular cortex area (PIC). In this article, we review the anatomy, connectivity, and function of PIVC and PIC and propose that the core of the human vestibular cortex consists of at least two separate areas, which we refer to together as PIVC+. We also review the organization in the nonhuman primate brain and show that there are parallels to the proposed organization in humans.


2012 ◽  
Vol 4 (1) ◽  
pp. 46-53
Author(s):  
Rahul T Chakor ◽  
Nishikant Eklare

ABSTRACT Background Vertigo as a symptom of cerebrovascular disease is relatively uncommon. All types of cerebrovascular diseases namely ischemia, infarction, hemorrhage can produce vertigo. Since, cerebrovascular disease is an emergency prompt recognition and treatment is necessary to prevent neurologic deficit and death. Among cerebrovascular diseases vertebrobasilar territory strokes commonly present with vertigo. Since, the term vertigo is used nonspecifically by patients this may lead to delay in diagnosis of these strokes. This article reviews the epidemiology of vertigo in cerebrovascular diseases and the various stroke syndromes associated with vertigo. Summary Cerebrovascular diseases in the vertebrobasilar territory have vertigo, imbalance, dizziness in addition to other symptoms and signs. Posterior inferior cerebellar artery, anterior inferior cerebellar artery, superior cerebellar artery and basilar artery territory strokes can present with true vertigo. A high index of suspicion of stroke in patients with vertigo and risk factors for stroke is essential. Other vascular causes of vertigo are small cerebellar hemorrhage, vestibular cortex stroke, rotational vertebral artery syndrome, transverse/sigmoid sinus thrombosis and vestibular paroxysmia. Conclusion Cerebrovascular disorders are estimated to account for 3 to 4% of patients with vertigo or dizziness. Early detection and treatment is necessary to prevent disability and death in these cases of vascular vertigo. How to cite this article Chakor RT, Eklare N. Vertigo in Cerebrovascular diseases. Int J Otorhinolaryngol Clin 2012;4(1):46-53.


2014 ◽  
Vol 155 (34) ◽  
pp. 1335-1343 ◽  
Author(s):  
Mónika Schulte-Altedorneburg ◽  
Dániel Bereczki

Cerebrovascular diseases are associated with a high incidence of psychiatric disorders. Depressive illness after stroke has been extensively investigated during the last three decades. Post-stroke depression is estimated to occur in 30–35% of the patients during the first year after stroke. Numerous studies have given information on its prevalence, pathogenesis, clinical course, treatment and prevention. Despite the high level of comorbidity, depressive symptoms appear to remain frequently unrecognized and untreated. This has a negative effect on the rehabilitation, quality of live, cognitive function and mortality of stroke patients. Orv. Hetil., 2014, 155(34), 1335–1343.


2017 ◽  
Vol 30 (7-8) ◽  
pp. 739-761 ◽  
Author(s):  
Ramy Kirollos ◽  
Robert S. Allison ◽  
Stephen Palmisano

Behavioural studies have consistently found stronger vection responses for oscillating, compared to smooth/constant, patterns of radial flow (the simulated viewpoint oscillation advantage for vection). Traditional accounts predict that simulated viewpoint oscillation should impair vection by increasing visual–vestibular conflicts in stationary observers (as this visual oscillation simulates self-accelerations that should strongly stimulate the vestibular apparatus). However, support for increased vestibular activity during accelerating vection has been mixed in the brain imaging literature. This fMRI study examined BOLD activity in visual (cingulate sulcus visual area — CSv; medial temporal complex — MT+; V6; precuneus motion area — PcM) and vestibular regions (parieto-insular vestibular cortex — PIVC/posterior insular cortex — PIC; ventral intraparietal region — VIP) when stationary observers were exposed to vection-inducing optic flow (i.e., globally coherent oscillating and smooth self-motion displays) as well as two suitable control displays. In line with earlier studies in which no vection occurred, CSv and PIVC/PIC both showed significantly increased BOLD activity during oscillating global motion compared to the other motion conditions (although this effect was found for fewer subjects in PIVC/PIC). The increase in BOLD activity in PIVC/PIC during prolonged exposure to the oscillating (compared to smooth) patterns of global optical flow appears consistent with vestibular facilitation.


2021 ◽  
Author(s):  
Zhi-Cong Ding ◽  
Fang-Fang Xu ◽  
Qi-Di Sun ◽  
Bin Li ◽  
Neng-Xing Liang ◽  
...  

Abstract Backgrounds: Post-stroke depression is the most common and serious neuropsychiatric complication occurring after cerebrovascular accidents, seriously endangering human health while also imposing a heavy burden on society. Even so, it is difficult to have drugs to contain the progression of the disease. It’s reported that Gan-Mai-Da-Zao decoction was effective to PSD, but it is unknown on its mechanism of action for PSD. In this study, we aimed to explore the possible mechanisms of action of Gan-Mai-Da-Zao decoction in the treatment of PSD using network pharmacology and molecular docking.Material and methods: We obtained the active components and their targets of all drugs from the public database TCMSP and published articles. Then, we collected the PSD-related targets from GeneCards and OMIM databases. Cytoscape 3.8.2 was applied to construct PPI and composite target disease networks. In parallel, the DAVID database was used to perform GO and KEGG enrichment analysis to obtain the biological processes involved in drug treatment diseases in vivo. Finally, molecular docking was used to verify the association between the main active ingredients and the targets.Results: The network pharmacological analysis of Gan-Mai-Da-Zao decoction for PSD identified 107 active ingredients with important biological effects, including quercetin, luteolin, kaempferol, naringenin, isorhamnetin, etc. A total of 203 potential targets for drug treatment of diseases were screened, including STAT3, JUN, TNF, TPT53, AKT1, EGFR, etc. They were found to be widely enriched in a series of signaling pathways such as TNF, HIF-1, and the Toll-Like receptor. Meanwhile, molecular docking analysis showed that the core active components were tightly bound to the core targets, further confirming their anti-PSD effects.Conclusion: This is a prospective study based on the integration and analysis of large data, using the technology of network pharmacology to explore the feasibility of Gan-Mai-Da-Zao decoction for the treatment of PSD, and successfully validated by molecular docking. It reflects the multi-component and multi-target characteristics of Chinese medicine, and more importantly, it also brings hope to the clinical treatment of PSD.


Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Bharath Chelluboina ◽  
Anil Kiran Chokkalla ◽  
Suresh L Mehta ◽  
Saivenkateshkomal Bathula ◽  
Robert J Dempsey ◽  
...  

The mechanistic role of Tenascin-C (TNC) in the pathogenesis of acute ischemic stroke is not known despite its prognostic association with cerebrovascular diseases. We currently observed that transient middle cerebral artery occlusion (MCAO) upregulated cerebral TNC mRNA and protein expression between 3h and 24h reperfusion in adult mice of both sexes. We then evaluated the effect of TNC knockdown on ischemic outcome in adult mice of both sexes by treating with either TNC siRNA or control siRNA (intravenous) at 5 min of reperfusion following transient MCAO. TNC siRNA treatment significantly reduced the post-ischemic TNC protein induction tested at 72h reperfusion compared with the sex-matched control siRNA treated cohorts (n=6/group/sex). TNC siRNA cohorts showed significantly improved post-stroke motor function identified by beam walk test and rotarod test between days 1 and 14 of reperfusion compared with the sex-matched control siRNA cohorts (n=7/group/sex). TNC siRNA cohorts of both sexes also showed decreased post-ischemic BBB disruption (evaluated with T1-weighted MRI with gadobenate dimeglumine as contrast agent) and reduced infarction (assessed with T2-weighted MRI) at 3 days of reperfusion compared with the sex-matched control siRNA treated cohorts (n =4/group for BBB and n =12/group/sex for infarct). At day 21 of reperfusion, the survival rate was observed to be higher in the TNC siRNA treated mice compared with the control siRNA treated mice (n =7/group/sex). These studies thus show that induction of TNC during the acute period after stroke might be a mediator of ischemic brain damage and its knockdown is neuroprotective. Importantly this effect is independent of sex. The study was funded by the Department of Neurological Surgery, Univ. of Wisconsin-Madison.


Author(s):  
Rocco Salvatore Calabrò ◽  
Letteria Spadaro ◽  
Placido Bramanti

2017 ◽  
Vol 43 (06) ◽  
pp. 591-598 ◽  
Author(s):  
Konstantinos Stavropoulos ◽  
Konstantinos Imprialos ◽  
Chrysoula Boutari ◽  
Michael Doumas ◽  
Sofia Bouloukou

AbstractStroke is considered among the most common causes of mortality and disability, leading to dramatic socioeconomic consequences. From a pathophysiologic perspective, enhanced blood viscosity due to increased hematocrit might be associated with stroke through impaired cerebral blood perfusion. This association has remained rather neglected during previous decades, but newly emerged as an epicenter of scientific interest due to the unexpected elevation of stroke rates with sodium-glucose cotransporter-2 inhibitors, a new class of hypoglycemic drugs with otherwise dramatic cardiovascular benefits. The purpose of this article is to review available data on the relation between stroke and hematocrit values. Data from large observational studies point toward an increased risk for stroke in individuals with elevated hematocrit. Data also suggest that the coexistence of increased hematocrit values and hypertension significantly enhance the risk of cerebrovascular events compared with each condition alone. Additionally, high hematocrit values seem related to worse survival outcomes in post-stroke patients. Collectively, the association between hematocrit and stroke seems to be strong and independent in high hematocrit values (>0.50) in both previously healthy individuals and post-stroke patients, but remains less clarified in patients with normal hematocrit values.


Sign in / Sign up

Export Citation Format

Share Document