Effect of Jiawei Tongqiao Huoxue decoction in basilar artery dolichoectasia mice through yes-associated protein/transcriptional co-activator with PDZ-binding motif pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: The Jiawei Tongqiao Huoxue decoction (JTHD), composed of Acorus calamus var. angustatus Besser, Paeonia lactiflora Pall., Conioselinum anthriscoides 'Chuanxiong', Prunus persica (L.) Batsch, Ziziphus jujuba Mill., Carthamus tinctorius L., Pueraria montana var. lobata (Willd.) Maesen & S.M.Almeida ex Sanjappa & Predeep, Zingiber officinale Roscoe, Leiurus quinquestriatus, and Moschus berezovskii Flerov, was developed based on Tongqiao Huoxue decoction in Wang Qingren's "Yilin Gaicuo" in the Qing Dynasty. It has the effect of improving not only the blood flow velocity of vertebral and basilar arteries but also the blood flow parameters and wall shear stress. Especially in recent years, the potential efficacy of traditional Chinese medicine (TCM) for the treatment of basilar artery dolichoectasia (BAD) has attracted great attention as there are still no specific remedies for this disease. However, its molecular mechanism has not been elucidated. To identify the potential mechanisms of JTHD will help to intervene BAD and provide a reference for its clinical application. AIM OF THE STUDY: This study aims to establish a mouse model of BAD and explore the mechanism of JTHD regulating yes-associated protein/transcriptional co-activator with PDZ-binding motif (YAP/TAZ) pathway for attenuating BAD mice development. MATERIALS AND METHODS: Sixty post-modeling C57/BL6 female mice were randomly divided into sham-operated, model, atorvastatin calcium tablet, low-dose JTHD, and high-dose JTHD groups. After 14 days of modeling, the pharmacological intervention was given for 2 months. Then, JTHD was analyzed by liquid chromatography-tandem mass spectrometry (LC-MS). ELISA was utilized to detect the changes in vascular endothelial growth factor (VEGF) and lipoprotein a (Lp-a) in serum. EVG staining was conducted to observe the pathological changes of blood vessels. TUNEL method was employed to detect the apoptosis rate of vascular smooth muscle cells (VSMCs). Micro-CT and ImagePro Plus software were used to observe and calculate the tortuosity index, lengthening index, percentage increase in vessel diameter, and tortuosity of the basilar artery vessels in mice. Western blot analysis was performed to detect the expression levels of YAP and TAZ proteins in the vascular tissues of mice. RESULTS: Many effective compounds such as choline, tryptophan, and leucine with anti-inflammation and vascular remodeling were identified in the Chinese medicine formula by LC-MS analysis. The serum levels of VEGF in the model mice decreased significantly while the levels of Lp-a increased obviously compared with those in the sham-operated group. The intima-media of the basilar artery wall showed severe disruption of the internal elastic layer, atrophy of the muscular layer, and hyaline changes of the connective tissue. Apoptosis of VSMCs added. Dilatation, elongation, and tortuosity of the basilar artery became notable, and tortuosity index, lengthening index, percentage increase in vessel diameter, and bending angle remarkably improved. The expression levels of YAP and TAZ protein in blood vessels elevated conspicuously (P < 0.05, P < 0.01). JTHD group markedly reduced the lengthening, bending angle, percentage increase in vessel diameter, and tortuosity index of basilar artery compared with the model group after 2 months of pharmacological intervention. The group also decreased the secretion of Lp-a and increased the content of VEGF. It inhibited the destruction of the internal elastic layer, muscular atrophy, and hyaline degeneration of connective tissue in basilar artery wall. The apoptosis of VSMCs was decreased, and the expression levels of YAP and TAZ proteins were abated (P < 0.05, P < 0.01). CONCLUSIONS: The mechanism of inhibition of basilar artery elongation, dilation, and tortuosity by JTHD, which has various anti-BAD effective compound components, may be related to the reduction in VSMCs apoptosis and downregulation of YAP/TAZ pathway expression.

Modified Protocol for Establishment of Intracranial Arterial Dolichoectasia Model by Injection of Elastase Into Cerebellomedullary Cistern in Mice.

Background and Purpose: This study aimed to construct an animal model of intracranial arterial dolichoectasia (IADE) applying the modified modeling protocol. Materials and Methods: Twenty five milliunits elastase and inactivated elastase were, respectively, injected into the cerebellomedullary cistern of 60 C57/BL6 mice which were divided into experimental group (EG, n = 30) and control group (CG, n = 30) by using a computer-based random order generator. The modified modeling protocol clarified these aspects including brain three-dimensional parameters of mouse head fixation, angle of head inclination, fixed position of taper ear, needle holding technique, needle entry depth, prevention of liquid drug back flow, and storage conditions of elastase. And it was observed for the following parts such as mortality, inflammatory factors, craniocerebral arteries scanning, vascular tortuosity index, artery diameter, pathology of the cerebrovascular. Results: Within differently surveyed stage, the total mortality of mice in EG was 20%. ELISA illustrated that the levels of matrix metalloproteinase-9 (MMP-9) and tumor necrosis factor α (TNF-α) in peripheral blood were increased significantly after modeling. Angiography indicated that 100% of IADE in EG were observed and the diameter and tortuosity index of the basilar artery were significantly increased (P < 0.01). EVG histological processing and staining showed the disrupted internal elastic lamina, the atrophied muscle layer, and the hyalinized connective tissue of the basilar artery with the vascular wall tunica media in EG. Micro-computed tomography reported that the craniocerebral arteries of the mice in EG were outstandingly elongated, tortuous, and dilated. Conclusion: The modified modeling protocol can reduce the mortality, improve the success rate, and provide a stable animal model for IADE.

Risk Factors for Long-Term Death After Medullary Infarction: A Multicenter Follow-Up Study.

Background and Purpose: We investigated the risk factors for death in patients with medullary infarction (MI) during a long-term follow-up. Methods: We retrospectively examined 179 consecutive patients (130 men and 49 women) who had clinical and MRI findings consistent with MI between February 2012 and January 2017 at three university hospitals. Long-term outcomes were assessed by telephonic interview. The clinical and radiological features and risk factors for poor outcomes (modified Rankin scale score ≥ 3, all-cause death) were analyzed. Results: Mean age of patients was 58.3 ± 12.8 years (range, 25-87); mean follow-up period after stroke onset was 42.7 ± 13.2 months (range, 24-78). Basilar artery (BA) stenosis >50% was more closely related to medial medullary infarction (MMI) than other types. There was greater frequency of ipsilateral vertebral artery hypoplasia (VAH) or V4AH and V4 occlusion in lateral MI than in other types. On rostro-caudal classification, middle (M)+dorsal (D) was most frequent, followed by the ventral (V)+M+D types. 21.2% patients showed poor long-term prognosis. Age ≥ 65 years, recurrent stroke, dysphagia, >50% BA stenosis, and ventral MI were risk factors for poor long-term prognosis. All-cause mortality rate was 10.6%; age ≥ 65 years, recurrent stroke, and dysphagia were risk factors for death in the long-term. Ventral MI and MMI+cerebellar infarction, as well as stroke mechanism of artery-to-artery embolism, were potential risk factors for death in the long-term. Pneumonia and recurrent stroke were major causes of death. Conclusions: Long-term poor outcomes of MI and all-cause mortality were not infrequent. Older age, recurrent stroke, and dysphagia were common risk factors for poor prognosis and death.

MMP-9, Vertebrobasilar Ectasia and Vertebral Artery Dominance in Vertigo or Dizziness Patients With Vascular Risk Factors.

Background and Purpose: Although vertebrobasilar ectasia (VBE) is diagnosed with increasing frequency, it is not clear whether this is because of altered hemodynamics caused by the effects of matrix metalloproteinases (MMPs) and/or vertebral artery dominance (VAD). Therefore, we investigate the relationship between plasma levels of MMPs and VBE in patients with vertigo or dizziness who also have vascular risk factors, in order to determine whether high levels of MMPs in VBE are independent of VAD. Methods: We prospectively studied 285 patients with vertigo or dizziness and at least one vascular risk factor. Plasma levels of MMPs, tissue inhibitor of metalloproteinases (TIMPs) and cathepsin L were measured. Subjects were classified as VBE-negative or VBE-positive, who were further classified based on the presence of VAD with magnetic resonance angiography. Acute ischemic stroke was screened by diffusion-weighted imaging, generally after bedside evaluation and the drawing of blood samples. Receiver operating characteristic (ROC) curves were applied to evaluate the utility of these potential biomarkers in predicting risk for ischemic stroke. Results: The prevalence of VBE in patients with vertigo or dizziness was 16.5%. Of the 82 patients with ischemic stroke, 14 strokes involved the cortex or subcortex. MMP-9 levels were significantly higher in the VBE-positive group than in the VBE-negative group (P = 0.022). There was a significant difference in the risk of posterior circulation ischemic stroke between the VBE-positive group and the VBE-negative group (P = 0.002). Levels of MMP-2 and cathepsin L tended to be higher in the VBE-negative group (P = 0.054, P = 0.060, respectively). Compared with the non-VAD subgroup, levels of MMP-2,-3,-9, TIMP-1,-2, and cathepsin L were similar in the VAD subgroup. ROC analysis showed that MMP-9 predicted risk for ischemic stroke (AUC = 0.582, 95%CI, 0.510-0.654, P = 0.030). Conclusions: MMP-9 was associated with VBE and independent of VAD. High levels of MMP-9 may predict risk for ischemic stroke in patients with vertigo or dizziness who also have vascular risk factors.

Association between Intracranial Arterial Dolichoectasia and Cerebral Small Vessel Disease and Its Underlying Mechanisms.

Intracranial arterial dolichoectasia (IADE), also known as dilatative arteriopathy of the brain vessels, refers to an increase in the length and diameter of at least one intracranial artery, and accounts for approximately 12% of all patients with stroke. However, the association of IADE with stroke is usually unclear. Cerebral small vessel disease (CSVD) is characterized by pathological changes in the small vessels. Clinically, patients with CSVD can be asymptomatic or present with stroke or cognitive decline. In the past 20 years, a series of studies have strongly promoted an understanding of the association between IADE and CSVD from clinical and pathological perspectives. It has been proposed that IADE and CSVD may be attributed to abnormal vascular remodeling driven by an abnormal matrix metalloproteinase/tissue inhibitor of metalloproteinase pathway. Also, IADErelated hemodynamic changes may result in initiation or progression of CSVD. Additionally, genetic factors are implicated in the pathogenesis of IADE and CSVD. Patients with Fabry's disease and late-onset Pompe's disease are prone to developing concomitant IADE and CSVD, and patients with collagen IV alpha 1 or 2 gene (COL4A1/COL4A2) and forkhead box C1 (FOXC1) variants present with IADE and CSVD. Race, strain, familial status, and vascular risk factors may be involved in the pathogenesis of IADE and CSVD. As well, experiments in mice have pointed to genetic strain as a predisposing factor for IADE and CSVD. However, there have been few direct genetic studies aimed towards determining the association between IADE and CSVD. In the future, more clinical and basic research studies are needed to elucidate the causal relationship between IADE and CSVD and the related molecular and genetic mechanisms.

Basilar Artery Tortuosity Is Associated With White Matter Hyperintensities by TIMP-1.

BACKGROUND AND PURPOSE: To test the hypothesis that the imbalance between matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) may play a potential role in bridging vertebrobasilar dolichoectasia (VBD) with lacunar infarction (LI) and white matter hyperintensities (WMH). METHODS: We studied 212 patients with vertigo who underwent multimodal magnetic resonance imaging (MRI) tests for VBD, LI, and WMH identification. We investigated biomarkers of VBD with magnetic resonance angiography (MRA) via various physical characteristics of the vertebrobasilar arteries (VBAs). Similarly, LI and WMH biomarkers were extracted using T2-weighted and fluid attenuated inversion recovery (FLAIR) images. We first determined which of these neuroimaging markers were significant identifiers of VBD, LI and the different grades of WMH. We then sought to draw potential mechanistic conclusions from these MRI-derived parameters, by associating the aforementioned biomarkers with MMP and TIMP serum levels in patient blood samples using non-parametric statistical tests. RESULTS: MMP-9 serum level was significantly higher in vertigo patients with VBAs dilation and basilar artery (BA) elongation compared to those with healthy arterial size, and the ratio of MMP-9/TIMP-1 level were higher in those patients. TIMP-1 level was also markedly higher in vertigo patients with BA tortuosity than those without BA tortuosity. The bending length (BL) of the BA was positively correlated with TIMP-1. The length, BL, and tortuosity index of the BA, as well as serum levels of TIMP-1 were greater in patients with higher WMH grades compared to those with low WMH grades. The vertebral artery and BA diameters, and the levels of MMP-2, -3, -9, TIMP-2 and cathepsin L were similar in patients with different WMH grades. CONCLUSION: In vertigo patients, we found various probably associations between MMP-9 and TIMP-1 with arterial alterations linked to both VBD and WMH that may help with the diagnosis and treatment of such diseases in the future.

Prevalence of Stroke and Hypoperfusion in Patients With Isolated Vertigo and Vascular Risk Factors.

Background and Purpose: The aim of this study was to determine the prevalence and associated factors of stroke and hypoperfusion among patients with isolated vertigo and vascular risk factors. Methods: We studied 157 patients with isolated vertigo who had undergone multimodal magnetic resonance imaging. Magnetic resonance angiography (MRA) was used to measure the diameters of vertebrobasilar arteries and to evaluate morphologic changes to vessels. Measurements obtained included length of the basilar artery and curvature index for the vertebral artery (VA). Perfusion-weighted imaging (PWI) was performed to determine relative cerebral blood flow, relative cerebral blood volume (rCBV), time to peak (TTP), and mean transit time for two mirror regions of interest (ROIs) in each map. Regional hypoperfusion of the cerebellum was considered significant when TTP and mean transit time (MTT) were present in ≥2 adjacent slices. Results: The prevalence of stroke in patients with isolated vertigo and vascular risk factors was 24.8% (n = 39). Visual assessment revealed cerebellar hypoperfusion in 57.6% (68/118) of non-stroke patients. Multivariate logistic regression indicated that diabetes mellitus (P = 0.049, OR = 2.758), VA stenosis or hypoplasia (P = 0.023, OR = 3.486), and relative TTP of cerebellum (P = 0.002, OR = 3.197) were independent risk factors for stroke and LVA curvature index (P = 0.026, OR = 2.049), VA stenosis and hypoplasia (P = 0.009, OR = 2.977) were independent risk factors for hypoperfusion. Conclusions: The prevalence of stroke and hypoperfusion is higher in patients with isolated vertigo and vascular risk factors, compared with matched controls. Potential risk factors include diabetes mellitus, VA stenosis or hypoplasia, and enlarged VA curvature index.

Perfusion by delayed time to peak in vertebrobasilar dolichoectasia patients with vertigo.

OBJECTIVE: To investigate the association between the perfusion magnetic resonance imaging (MRI) and vertebrobasilar dolichoectasia (VBD) in vertigo patients and at least one vascular risk factor. METHODS: We studied 289 patients with vertigo (spinning, swaying, nausea, vomiting, and unsteady gait) who performed multimode MRI. Maximum diameter and tortuous parameters of the basilar artery and vertebral arteries were calculated using magnetic resonance angiography. Relative cerebral blood volume (rCBV), relative cerebral blood flow (rCBF), mean transit time (MTT), and time to peak (TTP) maps were evaluated by dynamic susceptibility contrast-enhanced perfusion imaging. Association of perfusion MRI and VBD was evaluated by nonparametric tests and receiver-operating characteristic curve was constructed to predict posterior ischemic stroke in VBD patients. RESULTS: The prevalence of VBD was 26.6% (n = 77/289) in our study. Male gender was the risk factor of VBD by multivariate analysis. BA diameter was significant statistics between ischemic stroke and nonischemic stroke patients. TTP in bilateral lower cerebellum, superior cerebellum, bilateral pons, and occipital and temporal lobes region of interests was significantly delayed in VBD versus non-VBD patients, while rCBF, rCBV, and MTT parameters were not significant differences. TTP in the right temporal lobe delayed by 21.96 ms was the best predictive value and the mean TTP predictive threshold value in all ROIs was 22.67 ± 1.48 ms. INTERPRETATION: VBD leads to the hypoperfusion of posterior circulation territory characterized by delayed TTP. Delayed TTP in cerebellum, pons, and occipital and temporal lobes fed by vertebrobasilar arteries predicted the occurrence of posterior ischemic stroke in VBD patients.

Why does my patient's basilar artery continue to grow? A four-year case study of a patient with symptoms of vertebrobasilar dolichoectasia.

BACKGROUND: Vertebrobasilar dolichoectasia (VBD) is a clinical entity associated with ischemic stroke, compression of cranial nerves or brainstem, and hydrocephalus. There have been relatively few studies following the progression of VBD in patients presenting with a variety of diverse clinical features. CASE PRESENTATION: Here, we report a case study of a male with progressive VBD who was followed from November 2012 to December 2016. The patient had diagnosed hypertension for several years and suffered from left peripheral facial paralysis, recurrent ischemic attacks in the brainstem and cerebellum, obstructive hydrocephalus and frequent pneumonia. A series of cranial CT and multi-modal MRI scans were performed to explore the brain imaging features of the patient during follow-up. CONCLUSIONS: The presented case study suggests that aging, uncontrolled hypertension, arterial dissection and infection may contribute to the exacerbation of VBD and recurrent ischemic stroke.

A Preclinical Systematic Review of Ginsenoside-Rg1 in Experimental Parkinson's Disease.

To date, no drug has been proven to be neuroprotective or disease-modifying for Parkinson's disease (PD) in clinical trials. Here, we aimed to assess preclinical evidence of Ginsenosides-Rg1 (G-Rg1), a potential neuroprotectant, for experimental PD and its possible mechanisms. Eligible studies were identified by searching six electronic databases from their inception to August 2016. Twenty-five eligible studies involving 516 animals were identified. The quality score of these studies ranged from 3 to 7. Compared with the control group, two out of the 12 studies of MPTP-induced PD showed significant effects of G-Rg1 for improving the rotarod test (P < 0.01), two studies for improving the swim-score values (P < 0.01), six studies for improving the level of TH protein expression (P < 0.01), and two studies for increasing the expression of TH mRNA in the substantia nigra of mice (P < 0.01). The studies reported that G-Rg1 exerted potential neuroprotective effects on PD model through different mechanisms as antineuroinflammatory activities (n = 10), antioxidant stress (n = 3), and antiapoptosis (n = 11). In conclusion, G-Rg1 exerted potential neuroprotective functions against PD largely by antineuroinflammatory, antioxidative, and antiapoptotic effects. G-Rg1 as a promising neuroprotectant for PD needs further confirmation by clinical trials.

Vertebral Artery Hypoplasia and Posterior Circulation Infarction in Patients with Isolated Vertigo with Stroke Risk Factors.

BACKGROUND: We aimed in this study to investigate the prevalence of vertebral artery hypoplasia (VAH) in a population with isolated vertigo in association with stroke risk factors, to determine whether VAH is an independent risk factor for posterior circulation infarction (PCI). METHODS: We sequentially enrolled 245 patients with isolated vertigo with at least 1 vascular risk factor, who were divided into PCI and non-PCI groups, according to present signs of acute infarction on diffusion-weighted magnetic resonance imaging. All patients underwent magnetic resonance angiography and cervical contrast-enhanced magnetic resonance angiography to screen for VAH. Univariate and multivariate logistic regression analyses were performed to identify the significant risk factors for PCI. RESULTS: VAH was found in 64 of 245 patients (26%). VAH (odds ratio [OR] = 2.70, 95%confidence interval [CI] 1.17-6.23, P = .020), median stenosis of the posterior circulation (OR = 7.09, 95%CI = 2.54-19.79, P < .001), and diabetes mellitus (OR = 3.13, 95%CI 1.38-7.12, P = .006) were independent risk factors for PCI. The predominant Trial of Org 10172 in Acute Stroke Treatment subtype in our patients with isolated vertigo with PCI complicated by VAH was mainly small-artery occlusion. CONCLUSIONS: Our findings suggest that VAH is an independent risk factor for PCI in patients with isolated vertigo with confirmed risk from stroke.

Basilar artery hypoplasia associated with changes of brainstem potential, transcranial Doppler and perfusion-weighted imaging.

OBJECTIVE: The aim of this study was to observe brainstem hemodynamic alterations associated with basilar artery hypoplasia (BAH). METHODS: Nine hundred and fifty-two consecutive patients received emergency multimodal computed tomography; magnetic resonance imaging and magnetic resonance angiogram during the period of January 2011 to December 2014 were included. The vascular risk factors, brainstem auditory evoked potential (BAEP), blink reflex (BR), transcranial Doppler (TCD) and dynamic susceptibility contrast-enhanced perfusion-weighted imaging were completed. RESULTS: There was significant difference in the abnormal rates of TCD and BAEP between BAH and non-BAH patients. A positive correlation between basilar artery diameter and systolic velocity among BAH patients was suggested. V-wave value was used to predict posterior circulation infarction (PCI) with the sensitivity of 0.933 and specificity of 0.50 with the cutoff value of 5.97 s. Abnormal BR rate was also significantly different in BAH and non-BAH patients. The latency of R2 was used to predict PCI with the sensitivity of 0.933 and specificity of 0.50 with the cutoff value of 46.4 ms. The incidence of hypoperfusion was higher in BAH than non-BAH group and it was significant difference. CONCLUSION: BAH is closely associated with hemodynamic alterations within the pons, which might contribute to vascular vertigo due to regional hypoperfusion.

[Effect of different blood pressure control targets within 48 h after hypertensive cerebral hemorrhage on hematoma enlargement and prognosis].

OBJECTIVE: To study the effect of different blood pressure control targets on hematoma enlargement and prognosis in patients within 48 h after hypertensive cerebral hemorrhage (HCH). METHODS: Between January, 2013 and July, 2016, 102 patients with HCH were randomized into group A (51 cases) and group B (51 cases) with different systolic blood pressure (SBP) control targets within 48 h. The patients in group A were given early active antihypertensive treatment with SBP control target of 130-140 mm Hg; those in group B received standard antihypertensive treatment with SBP control target of 170-180 mm Hg. The changes in the volume of hematomas and the patients' prognosis were compared between the two groups. RESULTS: After 48 h of treatment, SBP, hematoma volume and the National Institutes of Health Stroke Scale (NIHSS) score were significantly lower and Glasgou Coma Scale (GCS) score was significantly higher in group A than in group B (P<0.01 or 0.05). After 30 days of treatment, the patients in group A showed significantly better indicators of treatment efficacy than those in group B (Z=2.331, P=0.020). The mortality rate was lower in group A than in group B, but the difference was not statistically significant (Χ2=2.772, P=0.096). CONCLUSION: Early active antihypertensive treatment is safe and feasible in patients with HCH and can reduce the enlargement of the hematomas, alleviate deterioration of neurological function, and improve the prognosis of the patients.

Vertebral artery hypoplasia, posterior circulation infarction and relative hypoperfusion detected by perfusion magnetic resonance imaging semiquantitatively.

Vertebral artery hypoplasia (VAH) has been considered a risk factor of posterior circulation infarction (PCI), especially in the territory of the posterior inferior cerebellar artery (PICA). But whether VAH is an independent risk factor for PCI remains uncertain and how VAH participates in the evolvement of PCI is still not clear either. Therefore, this study aims to examine whether VAH is an independent risk factor for PCI and evaluate the effect of VAH on the cerebral perfusion in the territory of the PICA detected by perfusion magnetic resonance imaging (MRI) semiquantitatively. Both univariate and multivariate analyses showed that VAH, hypertension and smoking were more frequent in patients with PCI than in patients without PCI. Perfusion MRI analysis found that there were remarkable differences in the frequency of the relative cerebral blood flow (rCBF) value ≤0.85 and the relative time to peak (rTTP) values between VAH patients without PCI and non-VAH patients without PCI. Our results indicated that VAH may be an independent risk factor for PCI, especially in the presence of hypertension and smoking and that a relative hypoperfusion associates with VAH that may contribute to the evolvement of the infarction in the PICA territory.

Basilar artery bending length, vascular risk factors, and pontine infarction.

BACKGROUND: Patients exhibiting basilar artery (BA) curvature (not dolichoectasia) are at an increased risk of posterior circulation ischemic stroke. In this study, pontine infarction patients were analyzed to assess the effect of BA bending length (BL) together with other vascular factors on pontine stroke risk. METHODS: Acute pontine infarction patients were divided into BA bending and non-BA bending groups by magnetic resonance angiography (MRA). Patients with BA bending who reported symptoms of dizziness or vertigo but who had not suffered brain infarction constituted the control group. The diameter of the vertebral artery (VA) and BL were measured using MRA. Based on the bilateral VA diameter data in vertebral artery-dominant (VAD) patients, the study participants were divided into three classes for VA diameter: class one, 0.30-0.80 mm (20 cases); class two, 0.81-1.37 mm (20 cases); and class three, 1.38-3.24 mm (20 cases). The measured BL in VAD cases allowed division of patients into three levels for BL: level one, 1.02-2.68 mm (21 cases); level two, 2.69-3.76 mm (20 cases); and level three, 3.77-7.25 mm (19 cases). Vascular risk factors were compared among the three groups. Correlations of BL and VA diameter differences were studied, and multivariate analysis was applied to search for predictors of ischemic stroke in BA bending patients. RESULTS: Among BA bending, non-BA bending, and control groups, VA dominance (VAD) proved to be a significant differentiator. For all three groups, a patient age of ≥ 65 years, the occurrence of hypertension, smoking, high homocysteine levels, high cholesterol, and a history of type 2 diabetes, were all statistically significant factors (P<0.05). After adjusting for other relevant factors, multivariate analysis shows that BL of level 3 was an independent risk factor for pontine infarction (OR=2.74; 95% CI, 1.27 to 4.48). Both BL and diameter differences between the VAs were positively correlated with risk with statistical significance (r=0.769, P<0.001). CONCLUSIONS: Both BL and diameter differences between the VAs are positively correlated with the risk of pontine infarction. When BA bending was coupled with other vascular risk factors, the probability of pontine infarction increased. BA bending with a BL greater than 3.77 mm was an independent predictor of pontine infarction.

Vertebral artery dominance, brainstem auditory evoked potential, and vertigo of vascular origin.

OBJECTIVE: Vertebral artery dominance (VAD) is defined when there is a significant difference between the diameters of the vertebral arteries (VAs). VAD may be a risk factor for vertigo of vascular origin. The objectives of this study were: (1) to investigate changes of brainstem auditory evoked potential (BAEP) in patients with vertigo caused by VAD through magnetic resonance; and (2) to understand the possible mechanism(s) by which VAD triggers vertigo of vascular origin. METHODS: This prospective study involved 64 patients with vertigo, including 35 patients with VAD (VAD group) and 29 without VAD (non-VAD group) as detected by head magnetic resonance angiography. Age, sex, and other clinical histories were comparable in both groups. The degree of vertigo was graded and BAEP examination was performed in each patient. BAEP changes as well as their correlations of BAEP with the dominant VA and basilar artery (BA) were analyzed in both groups. RESULTS: The rate of abnormal BA shapes was 60% in the VAD group compared with 34.5% in the non-VAD group (Chi-square = 4.135, P<0.05). The median BA curvature was higher in the VAD group than that in the non-VAD group, 3.67 and 1.73 mm, respectively (P<0.01). Peak latencies (I, III, and V) in the VAD group were longer than those in the non-VAD group (P<0.01), but the difference in the III did not reach statistical significance (t = 1.916, P>0.05). Interpeak latencies (III-V and I-V) were longer in the VAD group than those in the non-VAD group (P<0.05); there was no significant difference in the interpeak latencies of I-III (P>0.05). The III-V/I-III ratios were higher in the VAD group than those in the non-VAD group. The vertigo severity level was significantly higher in the VAD group than that in the non-VAD group (3.2 ± 1.0 versus 2.2 ± 0.7). The vertigo severity level correlated with VAD and every major anomaly index of BAEP; its correlations with III-V/I-III were remarkably significant (r = 0.617, P = 0.013). CONCLUSION: The incidence of abnormal BA shapes and abnormal BAEP, and the vertigo severity level were higher in VAD patients. Moreover, VAD was found to correlate with abnormal BAEP, suggesting that VAD contributed to vertigo of vascular origin.