Rong Zhao

Blood Pressure Reduction in the Acute Phase of an Ischemic Stroke Does Not Improve Short- or Long-Term Dependency or Mortality: A Meta-Analysis of Current Literature

Abstract The purpose of this study was to perform a meta-analysis of current literature to determine whether lowering blood pressure (BP) during the acute phase of an ischemic stroke improves short- and long-term outcomes. PubMed, Cochrane, and Embase were searched until September 5, 2014 using combinations of the search terms: blood pressure reduction, reduced blood pressure, lowering blood pressure, ischemic stroke, acute stroke, and intra-cerebral hemorrhage. Inclusion criteria were randomized controlled trial and patients with acute stroke (ischemic or hemorrhagic) treated with an antihypertensive agent or placebo. Outcome measures were change in systolic and diastolic BP (SBP, DBP) after treatment, and short- and long-term dependency and mortality rates. A total of 459 studies were identified, and ultimately 22 studies were included in the meta-analysis. The total number of participants in the treatment groups was 5672 (range, 6–2308), and in the control groups was 5416 (range, 6–2033). In most studies, more than 50% of the participants were males and the mean age was more than 60 years. The mean follow-up time ranged from 5 days to 12 months. As expected, treatment groups had a greater decrease in BP than control groups, and this effect was seen with different classes of antihypertensive drugs. Short-term and long-term dependency rates were similar between treatment and control groups (short-term dependency: pooled odds ratio [OR] = 1.041, 95% confidence interval [CI]: 0.936–1.159, P = 0.457; long-term dependency: pooled OR = 1.013, 95% CI: 0.915–1.120, P = 0.806). Short-term or long-term mortality was similar between the treatment and control groups (short-term mortality: pooled OR = 1.020, 95% CI: 0.749–1.388, P = .902; long-term mortality: pooled OR = 1.039, 95% CI: 0.883–1.222, P = 0.644). Antihypertensive agents effectively reduce BP during the acute phase of an ischemic stroke, but provide no benefit with respect to short- and long-term dependency and mortality.

Assessment of gray and white matter structural alterations in migraineurs without aura

BackgroundMigraine constitute a disorder characterized by recurrent headaches, and have a high prevalence, a high socio-economic burden and severe effects on quality of life. Our previous fMRI study demonstrated that some brain regions are functional alterations in migraineurs. As the function of the human brain is related to its structure, we further investigated white and gray matter structural alterations in migraineurs.MethodsIn current study, we used surface-based morphometry, voxel-based morphometry and diffusion tensor imaging analyses to detect structural alterations of the white matter and gray matter in 32 migraineurs without aura compared with 32 age- and gender-matched healthy controls.ResultsWe found that migraineurs without aura exhibited significantly increased gray matter volume in the bilateral cerebellar culmen, increased cortical thickness in the lateral occipital-temporal cortex, decreased cortical thickness in the right insula, increased gyrification index in left postcentral gyrus, superior parietal lobule and right lateral occipital cortex, and decreased gyrification index in the left rostral middle frontal gyrus compared with controls. No significant change in white matter microstructure was found in DTI analyses.ConclusionThe significantly altered gray matter brain regions were known to be associated with sensory discrimination of pain, multi-sensory integration and nociceptive information processing and were consistent with our previous fMRI study, and may be involved in the pathological mechanism of migraine without aura.

Predictive role of CHADS2 and CHA2DS2-VASc scores on stroke and thromboembolism in patients without atrial fibrillation: a meta-analysis

Abstract Objective: CHA2DS2-VASc is the extension of the CHADS2 score developed by Birmingham 2009. This risk stratification schema is often used in clinical setting when considering additional risk factors for developing stroke in AF patients. However, its role in the non-AF population is unknown. This study was designed to evaluate the accuracy of the CHADS2 and the CHA2DS2-VASc scoring systems. Methods: Studies designed for CHADS2 and CHA2DS2-VASc score in stratifying the risks for stroke development in non-AF patients were included. Results: Among the 114 studies identified, six trials were chosen finally and included for meta-analysis. The pooled diagnostic odds ratio (DOR) for CHADS2 and CHA2DS2-VASc was 2.86 (95% CI =1.83–4.28) and 2.80 (95% CI =1.83–4.28), respectively. CHA2DS2-VASc score was of better sensitivity than CHADS2 score (0.920 vs. 0.768). However, both scores were showed to have inherent heterogeneity and poor specificity. Conclusions: Though having good diagnostic accuracy, the clinical application of the CHADS2 and CHA2DS2-VASc scores in predicting risk of stroke development in non-AF patients still needs further validation. Key message The overall diagnostic accuracy of CHADS2 and CHA2DS2-VASc in stroke-risk stratification was good in patients with non-atrial fibrillation.

The sensorimotor network dysfunction in migraineurs without aura: a resting-state fMRI study

Migraine is a common recurrent neurological disorder combining nausea, vomiting, and hypersensitivities to visual, auditory, olfactory and somatosensory stimuli. However, the dysfunction of the sensorimotor network in migraineurs has not been well clarified. In the present study, we evaluated the dysfunction of the sensorimotor network in 30 migraineurs without aura and in 31 controls by combining regional homogeneity (ReHo), amplitudes of low-frequency fluctuation (ALFF) and degree centrality (DC) analysis methods based on resting-state fMRI. A seed-based functional connectivity (FC) analysis was used to investigate whether the dysfunctional areas within the sensorimotor network exhibited abnormal FC with other brain areas. Compared to the controls, the migraineurs without aura exhibited significantly smaller ReHo, ALFF and DC values in the primary somatosensory cortex (S1) and right premotor cortex (PMC). The migraineurs showed weaker FC between the S1 and brain areas within the pain intensity and spatial discrimination pathways and trigemino-thalamo-cortical nociceptive pathway. We proposed that the dysfunction of the S1 and PMC and the decreased FC between the S1 and brain areas in migraineurs without aura may disrupt the discrimination of sensory features of pain and affect nociception pathways, and would be involved in the dysfunctional mechanism in migraine.

Progressive Hemorrhagic Transformation Following Dual Antiplatelet Therapy

Dual antiplatelet therapy (DAT) is often used after endovascular interventional treatment to prevent the recurrence of a stroke. However, DAT may lead to cerebral hemorrhage. We describe two stroke patients with subacute progressive cerebral hemorrhagic transformation (HT) following DAT with aspirin and Plavix. One patient experienced HT 3 weeks after carotid artery stenting that was performed 3 days after an acute stroke; the other patient developed progressive HT within 4 weeks following emergent thrombectomy for acute occlusion of the inferior M2 branch of the right middle cerebral artery (MCA). The first patient was a 54-year-old male with a history of hypertension and smoking. He was admitted for acute cerebral infarction in the left temporoparietal lobe and received intravenous thrombolysis (Figure 1A). He was found to have significant stenosis in the proximal portion of the left internal carotid artery (ICA) (Figure 1B). Three days after the stroke, the patient underwent successful angioplasty (4 9 20 mm Sterling Monorail balloon, Boston Scientific, Natick, MA) and stenting (7 9 30 mm Wallstent, Boston Scientific, Natick, MA) of the stenotic left carotid artery (Figure 1C). One week after the procedure, the patient was discharged with partial motor aphasia, right facial palsy, and right limb hemiplegia (upper, grade 0/5; lower, grade 4/5). Aspirin (100 mg qd), Plavix (75 mg qd), and atorvastatin (20 mg qn) were used for secondary prevention. Three weeks after the procedure, the patient complained of dizziness, headache, nausea, and vomit(A) (B) (C)

Rivaroxaban does not influence hemorrhagic transformation in a diabetes ischemic stroke and endovascular thrombectomy model

Managing endovascular thrombectomy (ET) in diabetic ischemic stroke (IS) with novel anticoagulants is challenging due to putative risk of intracerebral hemorrhage. The study evaluates increased hemorrhagic transformation (HT) risk in Rivaroxaban-treated diabetic rats post ET. Diabetes was induced in male Sprague-Dawley rats by intraperitoneal injection of 60 mg/kg streptozotocin. After 4-weeks, rats were pretreated orally with 30 mg/kg Rivaroxaban/saline; prothrombin time was monitored. IS and ET was induced after 1 h, by thread-induced transient middle cerebral artery occlusion (tMCAO) that mimicked mechanical ET for proximal MCA occlusion at 60 min. After 24 h reperfusion, infarct volumes, HT, blood-brain barrier (BBB) permeability, tight junction at peri-ischemic lesion and matrix metalloproteinase-9 (MMP-9) activity was measured. Diabetic rats seemed to exhibit increased infarct volume and HT at 24 h after ET than normal rats. Infarct volumes and functional outcomes did not differ between Rivaroxaban and diabetic control groups. A significant increase in HT volumes and BBB permeability under Rivaroxaban treatment was not detected. Compared to diabetic control group, neither the occludin expression was remarkably lower in the Rivaroxaban group nor the MMP-9 activity was higher. Together, Rivaroxaban does not increase HT after ET in diabetic rats with proximal MCA occlusion, since Rivaroxaban has fewer effects on post-ischemic BBB permeability.

The Posterior Insula Shows Disrupted Brain Functional Connectivity in Female Migraineurs Without Aura Based on Brainnetome Atlas

Long-term headache attacks may cause human brain network reorganization in patients with migraine. In the current study, we calculated the topologic properties of functional networks based on the Brainnetome atlas using graph theory analysis in 29 female migraineurs without aura (MWoA) and in 29 female age-matched healthy controls. Compared with controls, female MWoA exhibited that the network properties altered, and the nodal centralities decreased/increased in some brain areas. In particular, the right posterior insula and the left medial superior occipital gyrus of patients exhibited significantly decreased nodal centrality compared with healthy controls. Furthermore, female MWoA exhibited a disrupted functional network, and notably, the two sub-regions of the right posterior insula exhibited decreased functional connectivity with many other brain regions. The topological metrics of functional networks in female MWoA included alterations in the nodal centrality of brain regions and disrupted connections between pair regions primarily involved in the discrimination of sensory features of pain, pain modulation or processing and sensory integration processing. In addition, the posterior insula decreased the nodal centrality, and exhibited disrupted connectivity with many other brain areas in female migraineurs, which suggests that the posterior insula plays an important role in female migraine pathology.

Repeated Transient Wallenberg's Syndrome: Probable Association with Ipsilateral Vertebral Artery Hypoplasia and Aortic Valve Disease

BACKGROUND Here we report a rare case of repeated transient Wallenbergs syndrome and discuss its mechanism. METHODS Case report and literature review. RESULTS A 57-year-old man was admitted for 1.5-month repeated transient Wallenbergs syndrome, including right-sided Horners syndrome, lower limb weakness, and paresthesia on the right side of the body and face. His symptom appeared mostly during physical activity. Symptoms occurred nearly everyday and lasted from 5 minutes to 30 minutes. His cranial magnetic resonance imaging (MRI) including diffusion-weighted MRI imaging was normal, and his cervical contrast-enhanced magnetic resonance angiography reflected right vertebral artery hypoplasia. Twenty-four-hour electrocardiogram and electroencephalography showed no abnormalities. Echocardiography showed aortic valve calcification with moderate aortic stenosis, moderate aortic insufficiency, and dilated aorta. Dual-antiplatelets or warfarin (international normalized ratio reached 2.07) were not effective to reduce the attacks. CONCLUSIONS Hemodynamic instability due to valve disease combined with right vertebral artery hypoplasia could lead to transient Wallenbergs syndrome. Antithrombotics are often ineffective for this kind of patients and the best therapy for them could be to cure their valve disease. Repeated transient Wallenbergs syndrome is rare and that caused by ipsilateral vertebral artery hypoplasia and severe valve disease has not been reported up till now to our knowledge, so it will widen the knowledge on etiologies of transient ischemic attacks and provide information and reference to cardiologists and neurologists in diagnosis and treatment for patients with similar clinical manifestations.

Delayed Shortening and Shifting of Carotid Wallstent

Carotid angioplasty and stenting (CAS) is a minimally invasive technique that is a reasonable alternative to carotid endarterectomy (CEA), especially in patients at high risk for surgery [1]. Although CAS is technically simple and is considered to be a low risk procedure, intracranial hemorrhage, distal embolization, transient hypotension, hyperperfusion syndrome, and other complications have been reported [2,3]. However, there have been few reported cases of delayed shortening of the Carotid Wallstent (Boston Scientific Corporation, Natick, MA, USA) used in the procedure. We report a case of delayed Carotid Wallstent shortening and shifting and discuss the possible causes of this complication. A 64-year-old male was admitted for inarticulacy and limb weakness of 1 month. The patient had a history of hypertension for 15 years (up to 205/130 mmHg) but was usually taking Adalat with good blood pressure control. He also had a history of smoking for more than 40 years (20 cigarettes/day) and drinking for decades (0.5 kg/day). On physical examination, the patient had mild facial and lingual paralysis of the right side; the rest of the neurological examination was normal. Brain MRI showed an acute cerebral infarct lesion in the right basal ganglia. Contrastenhanced magnetic resonance (MR) angiography showed a significant stenosis of the proximal segment of the right internal carotid artery (Figure 1A). A CAS procedure was performed under local anesthesia with embolic protection devices. Stent deployment was performed with a 7 9 30 mm self-expandable Carotid Wallstent (Figure 1B), and postdilatation was performed with a 4-mm balloon (Sterling, Boston Scientific, Natick, MA, USA) because of residual stenosis (Figure 1C). Three weeks after the operation, the patient developed diplopia; on examination, he had limited adduction of the left eye on right gaze. He had persistent mild facial and lingual paralysis of the right side. The patient did not have limb weakness, and the left Babinski sign was positive. Bultrasonography showed no stenosis or occlusion of either carotid artery. The patient was considered to be having another stroke. Medication for secondary prevention was continued. Ten months after the operation, the patient underwent cranial digital subtraction angiography (DSA) follow-up; the right Carotid Wallstent was found to have shortened and shifted to the common carotid artery (CCA), and there was mild intimal hyperplasia within the stent (Figure 1D). Shortening and shifting of the carotid artery stent have rarely been reported. The only previous report is from Yoon et al. [4] who reported that four patients who had received Carotid Wallstent implantation experienced delayed shortening and shifting of the Wallstents and restenosis. The Carotid Wallstent can be shortened or elongated to comply with the vessel diameter during implantation; however, such a phenomenon has rarely occurred after implantation. There are two possible causes for shortening of the Wallstent in this case. Firstly, the marked mismatch of diameters between the CCA and the internal carotid artery (ICA) may have induced the shortening of the stent. In our case, the CCA was approximately 7.7 mm in diameter, whereas the ICA diameter was 3.8 mm. This resulted in a rather conical-shaped Wallstent implantation. A slow further expansion of the Wallstent at the CCA level could have