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Vestibular migraine(VM)is a common vestibular disorder in which vertigo and migraine coexist,and visually induced vertigo is one of the typical vestibular symptoms of VM.The clinical manifestations of VM re-lated visual vertigo are various,which are affected by anxiety,motion sickness,age and other factors.Multiple mechanisms such as anatomical and physiological connections,gaze instability,visual vestibular integration defects,impaired sensory remodeling,sensitization of the central vestibular pathway,5-hydroxytryptamine and glutamate-glutamine cycle and other neurotransmitters may lead to VM-related visual vertigo.
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The comorbidities of vertebrobasilar dolichoectasia（VBD） and cerebral small vessel disease（CSVD） increase the poor prognosis of patients，and elucidating the mechanism underlying their comorbidities helps to explore effective treatment strategies. Therefore，based on the collateral disease theory and combining with the pathogenesis and research progress of traditional Chinese and Western medicine on the understanding of the two，this study proposes that both the disease locations are in the brain collaterals and the pathogenesis is deficiency in foundation and excess in symptoms. The main pathogenesis roots in the deficiency of original Qi and the emptiness of brain collaterals，which corresponds to the dysfunction of endothelial cells and neuro-endocrino-immune networks in modern medicine. The symptoms are cerebral blood stasis，occlusion of cerebral arteries and toxic lesion of cerebral arteries，corresponding to cerebrovascular atherosclerosis，hemodynamic changes，hypoperfusion and toxic metabolites-induced injury of white matter in modern medicine. Based on the collateral disease theory，exploring the common pathogenesis of the VBD and CSVD is expected to facilitate the establishment of TCM treatment scheme including the principles，methods and medicines，and improve the clinical prognosis of patients.
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ObjectiveTo establish a mouse model of basilar artery dolichoectasia （BAD） and explore the mechanism of modified Tongqiao Huoxuetang （JTQHX） in regulating BAD via phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） pathway. MethodSixty C57/BL6 female mice were randomized into sham operation （injected with 10 U·mL-1 inactivate elastase）， model， atorvastatin calcium tablets （2.6 mg·kg·d-1）， and low- and high-dose （crude drug 3.4， 17 g·kg-1·d-1， respectively） JTQHX groups. The mouse model of BAD was established by injection with 10 U·mL-1 elastase. After 14 days of modeling， the sham operation group and model group were administrated with equal volumes of pure water by gavage， and other groups with corresponding drugs for 2 months. The levels of interleukin-6 （IL-6） and calpain （LpA） in the serum were measured by enzyme-linked immunosorbent assay （ELISA）. Verhoeff 's Van Gieson （EVG） staining was employed to observe the pathological changes of blood vessels. Terminal-deoxynucleotidyl transferase mediated nick end labeling （TUNEL） was employed to examine the apoptosis rate of vascular smooth muscle cells （VSMCs）. Image Pro Plus was used to observe and calculate the curvature index， elongation length， percentage increase in vessel diameter， and curvature angle of the basilar artery vessels in mice. Western blot was employed to determine the expression levels of PI3K and Akt in the vascular tissue. ResultCompared with the sham operation group， the model group showed lowered IL-6 level （P<0.01）， no significant change in LpA level， increased apoptosis of VSMCs （P<0.01）， and increased curvature index， elongation length， percentage increase in vessel diameter， and curvature angle （P<0.01）. Furthermore， the modeling up-regulated the protein levels of PI3K and Akt in blood vessels （P<0.01） and aggravated the destruction of the inner elastic layer， atrophy of the muscular layer， and hyaline changes in the connective tissue of the medial membrane of the basilar artery wall. Compared with the model group， 2 months of treatment with JTQHX elevated the IL-6 level （P<0.01）， reduced the apoptosis of VSMCs （P<0.01）， decreased the curvature index， elongation length， percentage increase in vessel diameter， and curvature angle （P<0.05， P<0.01）， and down-regulated the protein levels of PI3K and Akt in blood vessels （P<0.01）. In addition， the treatment alleviated the destruction of the inner elastic layer， atrophy of the muscular layer， and hyaline changes in the connective tissue of the medial membrane of the basilar artery wall. ConclusionJTQHX inhibits the elongation， expansion， and curvature of basilar artery vessels and alleviates the pathological changes by reducing the apoptosis of VSMCs and down-regulating the expression of PI3K/Akt pathway.
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The core of diagnosing and treating diseases in traditional Chinese medicine lies in syndrome differentiation. The eight principles of syndrome differentiation serve as guidance for syndrome differentiation. As one of the eight principles of syndrome differentiation， the differentiation of deficiency and excess is the basic and critical method. Ischemic stroke is currently the leading cause harming the health of Chinese residents. Although the hypotheses about the cause of ischemic stroke have evolved from external wind to the later internal wind and to the modern theory of toxin damaging the brain collaterals， they all believe that this disease is rooted in internal deficiency and external excess. According to available studies， although stroke is characterized by complex pathogenesis and rapid progression of syndromes， the key cause evolution has a regularity， that is， from excess to deficiency. This article analyzes the historical evolution of the etiology， pathogenesis， and syndrome differentiation schemes of stroke. There are diverse schemes for the syndrome differentiation of stroke， which make it difficult to choose in clinical practice. In view of this problem， this paper puts forward a new approach of staging sequential treatment of ischemic stroke based on the differentiation of deficiency and excess according to the evolution law of the key cause of stroke. Furthermore， we conducted a randomized controlled study on 100 patients with ischemic stroke to evaluate this new approach. The results showed that the staging sequential treatment of ischemic stroke based on the differentiation of deficiency and excess demonstrated definite clinical efficacy. In addition， this article reviews the previous research results of our team and the research achievements of other teams to preliminarily explore the relationship between stroke syndromes and biomarkers， aiming to provide an objective basis for unveiling the pathogenesis of stroke. In summary， according to the key cause evolution （from excess to deficiency）， the treatment of ischemic stroke by stages based on differentiation of deficiency and excess can facilitate the rapid intervention and improve the clinical efficacy on ischemic stroke.
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Vertebrobasilar dolichoectasia (VBD) is a cerebrovascular variant disease. Researches have shown that further development of VBD may lead to severe disability and even death. The pathogenesis of VBD is still unclear, and there is no specific clinical prevention and treatment scheme. Therefore, establishing a stable and reliable animal model helps to further understand the pathophysiological mechanisms and potential therapeutic targets of VBD. This article reviews the establishment methods and research progress of the available VBD animal models.
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Vertebrobasilar dolichoectasia (VBD) is a disease characterized by the dilation, elongation, and tortuosity of the vertebrobasilar artery. Cerebral microbleeds (CMBs) are brain parenchymal injuries mainly caused by punctate microbleeds due to small vessel lesions. Recent studies have shown that VBD can increase the incidence rate of CMBs, but the correlation and pathophysiological mechanism of the two remain unclear. Multiple factors can induce VBD to accompany CMBs. A deep understanding of the causal relationship and related mechanisms between VBD and CMBs is helpful for the clinical prevention and treatment of such cerebrovascular diseases.
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Diet can be both a trigger and a treatment for migraine. The effects of alcohol, dairy products and pickled foods on migraine have been highly recognized. The effects of plant foods and caffeine on migraine currently have 2 sides. Ketogenic diet (KD), modified Atkins diet (MAD), and high n-3 fatty acid/low n-6 fatty acid diet can improve migraine through protecting nerves, improving mitochondrial function and energy metabolism, reducing calcitonin gene-related peptide (CGRP) levels, and inhibiting neuroinflammation. In this paper, the recent advance in the above content is summarized as follows.
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Persistent postural-perceptual dizziness (PPPD) is a chronic functional vestibular disease. Related studies have shown that PPPD patients often show high visual dependence in posture control or spatial orientation activities, and the symptoms are aggravated in visual motor stimulation or complex visual environment. The visual dependence of PPPD patients may be related to age factors, anxiety symptoms, visual-vestibular system interaction and neurotransmitter changes. A correct understanding of the relationship between vision and PPPD can provide more help for the clinical diagnosis and treatment of PPPD in the future. This article reviews the correlation and possible mechanism between visual factors and clinical symptoms of PPPD.
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Objective:To investigate the effect of magnetic resonance angiography (MRA) in evaluating the mouse model of vertebrobasilar dolichoectasia (VBD) induced by injection of elastase into cerebellomedullary cistern.Methods:Twenty-four male C57/BL6 mice were selected. The mice in the elastase group ( n=12) were injected in the cerebellomedullary cistern with 2.5 μl of phosphate buffer containing 25 mU elastase, and the mice in the saline control group ( n=12) were injected with the same volume of normal saline. MRA examination of the brains of living mice was performed 2 weeks after modeling. Successful modeling was defined as the basilar artery bending angle ≤170°, or the basilar artery bending length accounts for ≥10%, or the basilar artery deviated from the midline by more than 1 grade, or the percentage increase in artery diameter was ≥25%. Results:In the elastase group and the saline control group, 2 mice and 1 mouse did not wake up normally or died, respectively. The 11 surviving mice in the saline control group had no obvious vertebral artery and basilar artery abnormalities. The success rate of modeling in the 10 surviving mice in the elastase group was 80%, and the difference in the success rate between the two groups was statistically significant ( P<0.05). There were significant differences in mean basilar artery diameter (0.30 mm vs. 0.22 mm; P<0.05), mean basilar artery bending angle (115° vs. 170°; P<0.05), and proportion of mean basilar artery bending length (31% vs. 5%; P<0.05) of the surviving mice between the elastase group and the saline control group. Conclusion:MRA can better evaluate the mouse VBD model induced by elastase injection in the cerebellomedullary cistern.
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Posterior circulation ischemic stroke can be manifested as isolated vertigo, and the posterior circulation small infarcts often show early negative diffusion-weighted imaging, which is likely to cause misdiagnosis and missed diagnosis. Summarizing the characteristics and screening strategies of these patients can provide help for timely diagnosis and selection of effective treatment strategies.
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Cerebral small vessel disease (CSVD) is mainly manifested as lacunar infarction or lacunar space, white matter hyperintensities (WMHs), enlarged perivascular space (EPVS), cerebral microbleeds, and brain atrophy in imaging examination. Studies have shown that WMHs in the frontal lobe, occipital lobe, lateral ventricle, and basal ganglia are the important causes of dizziness/vertigo. The frequency of dizziness/vertigo symptoms increases with the worsening of WMHs. In addition, subcortical infarction, EPVS, and brain atrophy are also closely associated with dizziness/vertigo. Nerve conduction pathway damage, inflammatory infiltrating damage, vestibular degenerative lesions, mental and psychological disorders, and insufficient perfusion of blood vessels associated with large/small vessel disease may be the important ways for triggering dizziness/vertigo in CSDV. Early identification and diagnosis of CSVD-related dizziness/vertigo may contribute to the targeted prevention and treatment.
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Objective To explore the effects of vertebral artery hypoplasia (VAH)on falsenegative rates with MRI in isolated acute vestibular syndrome (AIVS) patients with small posterior circulation small infarcts (infarct diameter ≤ 10 mm by DWI).Methods A total of 224 AIVS patients with at least one stroke risk factor (defined as high-risk AIVS)were consecutively recruited.Head impulse,nystagmus and test-of-skew(HINTS),brainstem auditory evoked potential (BAEP),and blink reflex(BR)were performed as soon as possible ahead of MRI.Another MRI was carried out in those with negative findings on the first imaging but suspected of a central lesion based on HINTS + BAEP + BR.Patients were divided into a VAH group and a non-VAH group.Results Of the 98 cases with posterior circulation infarcts,37 cases were small infarcts,including 16 in the VAH group(16/61,26.2％)and 21 in the non VAH group(21/163,12.9％),with a significant difference between the groups(x2 =4.58,P ＜ 0.05).Nine VAH patients (9/16,56.3 ％)and 4 non-VAH patients(4/21,19.0％)presented false negative results on cranial MRI-DWI,and the difference was also statistically significant(x2 =6.23,P＜0.001).HINTS + BAEP + BR showed a higher sensitivity than early MRI in identifying small infarcts(VAH group:100.0％ vs.44.0％ or 7/16,U=6.41,P＜0.001;non-VAH group:100.0％ vs.81.0％ or 17/21,U=4.46,P＜0.0S).V wave peak latency,Ⅲ-Ⅴ and Ⅰ-Ⅴ wave interpeak latency,and the latency of R1,R2,and R2' in the VAH group were longer than in the non-VAH group(each P＜0.05).Conclusions When VAH is present in high-risk AIVS patients,small infarcts are common,with high false-negative rates on MRI-DWI.HINTS + BAEP + BR may help identify small infarcts and thus improve diagnostic sensitivity.
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Objective To explore the pathological process of MR imaging and clinical characteristics of bilateral Wallerian degeneration (WD) in the middle cerebellar peduncles after pontine infarction.Methods The present article reported one patient with paramedian pontine infarction who complicated bilateral WD in the middle cerebellar peduncles after 6 months;the major data included multimode MR imaging,brainstem auditory evoked potential and blink reflex.And then,these English and Chinese literature which reported 16 patients were reviewed together.The clinical,pathology and imaging characteristics of the 17 patients were summarized.Results Seventeen patients were all paramedian pontine infarction before finding WD:5 were on the right side and 11 were on the left side and one was bilateral side.When WD was found,original symptoms of pontine infarction were aggravated in 4 patients,one appeared dizziness and 12 were without symptoms.Thirteen patients had good prognosis,and the other 4 patients involved a poor prognosis because of severe primary lesions.Wallerian degeneration were found fiom 3 weeks to 33 weeks:2 were found DWI high signal in the bilateral middle cerebellar peduncles within four weeks after pontine infarction which attributed to first stage ofWD;4 had high MRI T2 signal close to 14 weeks which were in the second stage of WD;there were 11 with high T2 and FLAIR signal,low or equal apparent diffusion coefficient signal within 16 weeks after pontine infarction which were in the third stage of WD.No cases were in the fourth stage of WD.Conclusions Bilateral symmetry WD in the middle cerebellar peduncles is easily consolidated unilateral paramedian pontine infarction.The majority of these patients can be free for clinical symptoms and MR imaging features are usually in stage 2 and stage 3 of WD.These conditions have good clinical outcomes and should be paid more attention and avoided inappropriate treatments.
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Purpose To analyze the hemodynamic characteristics of brain stem in patients with basilar artery hypoplasia (BAH) by magnetic resonance perfusion-weighted imaging (PWI).Materials and Methods According to the inclusion and exclusion criteria,51 patients with BAH were selected as the BAH group,and 79 patients without BAH were selected as the non BAH group.All patients were examined by MRI,3D-TOF and PWI,and magnetic resonance angiography was acquired after the three examinations.The regional cerebral blood flow (rCBF),regional cerebral blood volume (rCBV),regional mean transit time (rMTT) and time to peak (TTP) values of pontine area were measured.Results The rCBF value of the BAH group [(17.10±6.52) ml/(100 g · min)] was significantly lower than that of the non BAH group [(29.06± 13.32) ml/(100 g · min)] (P＜0.05);the rCBV value of the BAH group [(1.41 ±0.26) ml] was significantly lower than that of the non BAH group [(2.62± 0.82) ml] (P＜0.05);the TTP value of the BAH group [(6.14± 1.31) s] was significantly higher than that of the non BAH group [(5.39 ± 1.08) s] (P＜0.05);the rMTT value of the BAH group [(20.78±3.48) s] was significantly higher than that of the non BAH group [(19.01 ±2.39) s] (P＜0.05).TTP was the most sensitive index of cerebral perfusion injury,and the incidence of TTP extension was 41.18％ in the BAH group.Conclusion PWI can detect the abnormal cerebral hemodynamics in patients with BAH,which provides the basis for the timely treatment and prevention of irreversible injury in the ischemic area of the brain.
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Objective To study the associations of acute cerebral infarction after spontaneousintracerebral hemorrhage (ICH) with white matter lesions (WMLs),cerebral artery stenosis and bloodpressure (BP) variability.Methods One hundred and fifty-five acute ICH patients,consecutivehospitalized within 24 h of onset from March 2012 to September 2015,were chosen;they were dividedinto infarction after ICH group and non-infarction after ICH group according to hyperintensities remotefrom the hematoma by magnetic resonance diffusion-weighted imaging (DWI) within 4 weeks of onset;according to positions of hemorrhage,they were divided into lobar hemorrhage group and non-lobarhemorrhage group;according to reduction range of mean arterial pressure (MAP) one h within admission,they were divided into intensive BP lowering group (MAP lowering by ≥20％) and non-intensive BPlowering group (MAP lowering＜20％).The clinical and radiological characteristics were analyzed toinvestigate the role of WMLs,cerebral artery stenosis and BP variability in acute cerebral infarction after spontaneous ICH.Results Ischcmic infarcts were detected in 36 of 155 patients (23.2％),mostly located at ipsilateral subcortical cortex;80.6％ of them were asymptomatic infarct and 66.7％ of them were lacunar infarcts.Positions of hemorrhage and severity of leukoaraiosis were significantly different between infarction after ICH group and non-infarction after ICH group (P＜0.05),while the cerebral artery stenosis was not significantly different between the two groups (P＞0.05).Stratified analysis showed that leukoaraiosis in patients from infarction after lobar ICH group was significantly severer than that in those from non-infarction after lobar ICH group (P＜0.05),and the cerebral artery stenosis in patients with infarction after non-lobar ICH was significantly severer than that in those with non-infarction after non-lobar ICH (P＜0.05).Intensive BP lowering patients with cerebral artery stenosis ≥ 50％ group had significantly increased risks of acute ischemic infarcts as compared with intensive BP lowering patients with cerebral artery stenosis＜50％ group,non-intensive BP lowering patients with cerebral artery stenosis ≥ 50％ group,and non-intensive BP lowering patients with cerebral artery stenosis＜50％ group,respectively (P＜0.05).Multivariate Logistic regression analysis showed that lobar hemorrhage and moderate to severe leukoaraiosis were independent risk factors of cerebral infarction after ICH (OR=2.484,95％CI:1.037-5.953,P=0.041;OR=2.426,95％CI:1.045-5.629,P=0.039).Conclusion Cerebral infarction after ICH is mainly associated with cerebral small vessel diseases,intensive BP lowering is associated with high risk of acute ischemic infarcts in patients with atherosclerotic large artery stenosis,and individualized BP control may maximumly reduce secondary brain injury after ICH.
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Basilar artery hypoplasia (BAH) has been paid less attention to in the past.However,the increased detection rate makes the clinical significance of BAH to be gradually recognized.BAH have interaction with vascular risk factors,and this may promote the occurrence of ischemic events in posterior circulation.Brain evoked potential can be used as an important means for early detection of this pathophysiological events.The depth study of pathological significance of BAH helps to deepen the understanding of the mechanisms of posterior circulation ischemic events.
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Vertebrobasilar dolichoectasia(VBD ) can increase the risk of stroke. Significant expansion, elongation and tortuosity of the vertebrobasilar arteries are the main morphology manifestations of VBD. However, there is no consensus on the quantitative imaging assessment of VBD. Many studies showed that some quantitative parameters, such as basilar artery length and bending length, basilar angulation, vertebral tortuosity index can be used for the quantitative imaging assessment of VBD.
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Objective To investigate the clinical risk factors of vertebral artery origin tortuosity and its impact on vascular vertigo. Methods Totally 206 inpatients in Department of Neurology were divided into tortuous group (n=137) and non-tortuous group (n=69).Clinical risk factors of cerebral vascular disease,vertigo scales and days of treatment relieve were recorded.Total cholesterol (CH),low density lipoprotein cholesterol (LDL-C),homocysteic acid (Hcy) and high sensitivity Creactive protein (hsCRP) were detected.Cervical computer tomography angiography (CTA) and contrast enhancement magnetic resonance angiography (CEMRA) were completed.The risk factors of vertebral artery origin tortuosity were analyzed with multiple logistic regression analysis. Results Vertebral artery dominance was much more in tortuous group than non-tortuous group(x2 =2.496,P＜0.01).Vertigo scales from 1 to 5 appeared in 17 cases,36 cases,79 cases,4 cases,1 case,respectively,and days of treatment relieve were 1-10 d in tortuous group,hut the corresponding data was 18 cases,35 cases,10 cases,3 cases,1 case and 1-6 d in non-tortuous group with statistical significance between the two groups(t=2.014,2.849,P＜0.01).The distinctions were found in age more than 65 years,hypertensive disease,high LDL-C,diabetes mellitus,smoking,stroke history,vertebral artery dominance and cervical spondylosis between tortuous group and non-tortuous group(x2=7.498,5.182,3.724,10.46,6.883,2.748,4.496,8.265,all P＜0.05).Age more than 65 years (95％CI:5.36-18.23,OR=4.84),hypertensive disease(95 ％ CI:2.79-16.45,OR=3.21),vertebral artery dominance(95％ CI:3.25-13.49,OR =5.48) and cervical spondylosis (95％ CI:4.38-21.28,OR=3.57) were high clinical risk factors. Conclusions Patients with vertebral artery origin tortuosity present with higher vertigo scales and longer days of treatment relieve.Age more than 65 years,hypertensive disease,vertebral artery dominance and cervical spondylosis are clinical risk factors for vertebral artery origin tortuosity.
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With the development of neuroimaging the detection rate of basilar artery tortuosity is significantly high.The occurrence and development processes of basilar artery tortuosity are affected by age,basilar artery length,vertebral artery dominance,and other factors.Basilar artery tortuosity may influence the blood supply of posterior circulation and cause brainstem and cranial nerve pressure leading to clinical symptoms.
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Vascular vertigo is a common vertigo.Vertebral artery dominance is a vascular phenomenon,and its mechanism remains unclear.It causes basilar artery changes and hemodynamic changes in posterior circulation.Vertebral artery dominance may trigger vascular vertigo through a variety of mechanisms.