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Vertical one-and-a-half syndrome (VOHS) is an uncommon presentation resulting from a unilateral thalamomesencephalic stroke with involvement of the rostral interstitial nucleus of the medial longitudinal fasciculus and posterior commissure. The artery of Percheron (aPe) is a branch of the posterior cerebral artery (PCA) and it is a variant that arises as a solitary trunk supplying both medial thalami and upper midbrain. A 78-year-old female patient, presented at the hospital emergency with approximately 12 hours of sudden onset of diplopia, associated with dizziness. Neurological exam revealed torsional nystagmus associated with bilateral upgaze palsy with limitation of infraduction on the left. We describe a rare case of VOHS associated with ischemic alterations at the MRI suggesting an aPe impairment. The conjugate gaze control lies anatomically at the midbrain at the central nervous system (CNS). This report describes a rare type of VOHS and brings a new insight on a possible aPe topography possibly causing this clinical presentation.

Background: Extracranial-intracranial (EC-IC) arterial bypass has been used in the treatment of various cerebrovascular ischemic disease due to atherosclerosis or Moyamoya disease, skull base tumors encasing large IC artery or complex IC aneurysms. Aim: The aim is to analyze surgical technique (EC-IC bypass) and its outcome with intraoperative use of dual image video angiography (DIVA) and Doppler ultrasound. Materials and Methods: We studied in this article a series of 23 patients operated in Banbuntane Hotokukai Hospital, Fujita Health University, for which a superficial temporal artery-middle cerebral artery anastomosis was done for steno-occlusive disease, giant IC aneurysm or Moyamoya disease. The study was conducted between 2018 and 2020. We used dual-image video angiography (DIVA) and Doppler ultrasound to assess the luminal patency of anastomosis during the procedure. Results: In this study, three patients presented with Moyamoya disease, 4 had aneurysm, whereas 16 patients presented with the vascular steno-occlusive disease. The patients were divided into three categories (steno-occlusive disease, Moyamoya, and flow replacement for giant aneurysm). Dual image video angiography, along with intraoperative Doppler, helped us in the assessment of luminal patency of the anastomosis. Conclusion: Hemodynamic recovery after cerebrovascular bypass brings about a better outcome in ischemic stroke. The result of surgery improves with proper selection of patients with hemodynamic impairment (in Stage 2). With various modalities such as intraoperative Doppler, DIVA (Dual-image Video Angiography) and improved surgical techniques may aid in the reduction of complications and improve clinical outcome.

Vessel wall imaging has been increasingly used to characterize plaque beyond luminal narrowing to identify patients who may be at the highest risk of cerebrovascular ischemia. Although detailed plaque information can be obtained from many imaging modalities, CTA is particularly appealing for carotid plaque imaging due to its relatively low cost, wide availability, operator independence, and ability to discern high-risk features. The present Review Article describes the current understanding of plaque characteristics on CTA by describing commonly encountered plaque features, including calcified and soft plaque, surface irregularities, neovascularization, and inflammation. The goal of this Review Article was to provide a more robust understanding of clinically relevant plaque features detectable on routine CTA of the carotid arteries.

Cerebrovascular ischemia from intracranial atherosclerosis remains difficult to treat. Although current revascularization procedures, including intraluminal stents and extracranial to intracranial bypass, have shown some benefit, they suffer from perioperative and postoperative morbidity. To address these limitations, here we developed a novel approach that involves gluing of arteries and subsequent transmural anastomosis from the healthy donor into the ischemic recipient. This approach required an elastic vascular sealant with distinct mechanical properties and adhesion to facilitate anastomosis. We engineered two hydrogel-based glues: an elastic composite hydrogel based on methacryloyl elastin-like polypeptide (mELP) combined with gelatin methacryloyl (GelMA) and a stiff glue based on pure GelMA. Two formulations with distinct mechanical characteristics were necessary to achieve stable anastomosis. The elastic GelMA/mELP composite glue attained desirable mechanical properties (elastic modulus: 288 ± 19 kPa, extensibility: 34.5± 13.4%) and adhesion (shear strength: 26.7± 5.4kPa) to the blood vessel, while the pure GelMA glue exhibited superior adhesion (shear strength: 49.4± 7.0kPa) at the cost of increased stiffness (elastic modulus: 581 ± 51 kPa) and reduced extensibility (13.6± 2.5%). The in vitro biocompatibility tests confirmed that the glues were not cytotoxic and were biodegradable. In addition, an ex vivo porcine anastomosis model showed high arterial burst pressure resistance of 34.0± 7.5kPa, which is well over normal (16 kPa), elevated (17.3kPa), and hypertensive crisis (24 kPa) systolic blood pressures in humans. Finally, an in vivo swine model was used to assess the feasibility of using the newly developed two-glue system for an endovascular anastomosis. X-ray imaging confirmed that the anastomosis was made successfully without postoperative bleeding complications and the procedure was well tolerated. In the future, more studies are required to evaluate the performance of the developed sealants under various temperature and humidity ranges.

The article presents data on the frequency and structure of comorbid pathology in patients with inferior wall myocardial infarction with right ventricular involvement. Its relationship with the clinical course of myocardial infarction in the acute period was studied. It was shown that patients with inferior wall myocardial infarction with right ventricular involvement have a high comorbid load. It was revealed that a more severe course of the acute period of myocardial infarction in these patients was associated with chronic cerebrovascular ischemia, fatty liver, chronic heart failure I–IIa stages, type 2 diabetes mellitus and obesity.

The public health sector faces a huge challenge as a result of the high prevalence and burden of disability caused by ischemic cardio-cerebrovascular disease (CVD) and depression. Although studies have explored the underlying mechanisms and potential therapies to address conditions, there is no treatment breakthrough, especially for depression which is highly influenced by social stressors. However, accumulating evidence reveals that CVD and depression are correlated and share common risk factors, particularly obesity, diabetes, and hypertension. They also share common mechanisms, including oxidative stress (OS), inflammation and immune response, cell death signaling pathway, and microbiome-gut-brain axis. This review summarizes the relationship between ischemic CVD and depression and describes the interactions among common risk factors and mechanisms for these two diseases. In addition, we propose that OS mediates the crosstalk between these diseases. We also reveal the potential of antioxidants to ameliorate OS-related injuries.

Background: Transient Ischemic Attack (TIA) (1) is a neurological dysfunction of transient cerebrovascular ischemia, which is more common in clinical practice. The risk of further progression to ischemic stroke after a higher TIA can be used as a strong early warning signal of cerebral infarction. Objectives: To explore the correlation between stromal cell-derived factor 1 (SDF-1) and the prognosis of TIA. Methods: A number of 65 patients with TIA were collected, the ABCD2 clinical risk prediction score was implemented, relevant tests and nuclear magnetic resonance imaging (MRI) were performed, and the SDF-1 was recorded in serum levels. End-point events were selected in patients after cerebral infarction in the short term. The statistical analysis method was used to evaluate TIA short-term development for the occurrence of cerebral infarction after risk, the severity of serum level of SDF-1, and infarction. Results: Based on the results, the high-risk group, middle-risk group, and low-risk group had statistically significant differences in serum SDF-1 levels (F=3.820; P

Stroke is the leading cause of disability and mortality worldwide. After an acute cerebrovascular ischemia, recurrent vascular events, including recurrent stroke or transient ischemic accidents (TIA), occur in around 20% of cases within the first 3 months. In order to minimize this percentage, antiplatelet therapy may play a key role in the management of non-cardioembolic cerebrovascular events. This review will focus on the current evidence of antiplatelet therapies most commonly discussed in practice guidelines and used in clinical practice for the treatment of stroke/TIA complications. The antiplatelet therapies most commonly used and discussed are as follows: aspirin, clopidogrel, and ticagrelor.

Background: A correlation between stroke and cervical manipulation in the neck is reported in the literature with increasing frequency, and each new publication seems to rekindle the debate. The manipulations in the cervical region is potentially dangerous for arterial vessels. The aim of this work is to analyze the incidence of these events in the experience of a center with high volume surgery, in which emergency interventions are performed for acute cerebrovascular Ischemia. Methods: Data were collected regarding patients undergoing carotid endarterectomy surgery for neurological symptoms of cerebrovascular insufficiency over a seven-year period. Results: The intervention was conducted urgently in 66 cases for acute symptoms (7.6%) with a median symptom interval / CEA: 39.4 ± 5.4 h) in 32 cases for hemispheric transient ischemic attack, while in 34 for minor stroke. Only in 1 case (1.5%) did a condition of severe spondyloarthrosis of the cervical spine occur in acute carotid plaque in C4-C5. In another case (1.5%) a cervical trauma caused by beatings is documented. Conclusions: Manipulations of the neck and cervical spine can rarely cause or contribute to worsening neurological symptoms, however they should always be considered.

Traumatic injuries of the cervical carotid and vertebral arteries, collectively referred to as blunt cerebrovascular injury (BCVI), can result in significant patient morbidity and mortality, with one of the most feared outcomes being cerebrovascular ischemia. Systematic imaging-guided screening for BCVI aims for early detection to guide timely management. In particular, accurate detection of the severity and grade of BCVI is paramount in guiding initial management. Furthermore, follow-up imaging is required to decide the duration of antithrombotic therapy. In this article, classification of the grades of BCVI and associated imaging findings will be outlined and diagnostic pitfalls and mimickers that can confound diagnosis will be described. In addition, updates to existing screening guidelines and recent efforts of criteria modification to improve detection of BCVI cases will be reviewed. The advent of postprocessing tools applied to conventional computed tomography (CT) angiograms and new diagnostic tools in dual energy CT for improved detection will also be discussed.

Cerebral ischemia is a very rare and harmful complication of ultrasound-guided foam sclerotherapy for treatment of varicose veins. This case describes a documented cerebrovascular ischemia in Broca’s area following ultrasound-guided foam sclerotherapy. Less than one hour after intravenous injection of 10 ml of sclerosing foam, an otherwise healthy woman experienced aphasia without any other signs of neurological changes. When she arrived home, a complete inability to talk was observed. The event was misdiagnosed by another doctor as an allergic reaction. Next morning she came to the office to report the allergic reaction, where an appropriate diagnosis was made. She recovered just two days after the injection, but signs of recent cerebral ischemia were seen in Broca’s area on magnetic resonance and transesophageal bubble study echocardiogram revealed a patent foramen ovale. Although rare, we must make great effort to prevent these events instead of treating them.

BACKGROUND: CTA is a widely available imaging examination that may allow the evaluation of high-risk carotid plaque features. PURPOSE: Our aim was to evaluate the association between specific carotid plaque features on CTA and ipsilateral cerebrovascular ischemia. DATA SOURCES: We performed a systematic review of Ovid MEDLINE, Ovid Embase, Scopus, and the Cochrane Library from inception to March 2016 for articles that evaluated the relationship between CTA-detected carotid plaque features and ischemic events, defined as ipsilateral ischemic stroke or transient ischemic attack. STUDY SELECTION: Sixteen studies were ultimately included after screening 12,557. DATA ANALYSIS: Two readers recorded data from each study and assessed the study quality with all disagreements resolved by a third reader. A random-effects OR was used to evaluate the association between cerebrovascular ischemia and each of the evaluated plaque features. DATA SYNTHESIS: We found significant positive relationships with cerebrovascular ischemia for the presence of soft plaque (OR, 2.9; 95% CI, 1.4–6.0), plaque ulceration (OR, 2.2; 95% CI, 1.4–3.4), and increased common carotid artery wall thickness (OR, 6.2; 95% CI, 2.5–15.6). We found a significant negative relationship between calcified plaque and ipsilateral ischemia (OR, 0.5; 95% CI, 0.4–0.7). LIMITATIONS: We found heterogeneity in the existing literature secondary to lack of standardized plaque features and clinical definitions. CONCLUSIONS: Soft plaque, plaque ulceration, and increased common carotid artery wall thickness on CTA are associated with ipsilateral cerebrovascular ischemia, while calcified plaque is negatively associated with downstream ischemic events.

The canonical transient receptor potential channels (TRPCs) constitute a series of nonselective cation channels with variable degrees of Ca2+ selectivity. TRPCs consist of seven mammalian members, TRPC1, TRPC2, TRPC3, TRPC4, TRPC5, TRPC6, and TRPC7, which are further divided into four subtypes, TRPC1, TRPC2, TRPC4/5, and TRPC3/6/7. These channels take charge of various essential cell functions such as contraction, relaxation, proliferation, and dysfunction. This review, organized into seven main sections, will provide an overview of current knowledge about the underlying pathogenesis of TRPCs in cardio/cerebrovascular diseases, including hypertension, pulmonary arterial hypertension, cardiac hypertrophy, atherosclerosis, arrhythmia, and cerebrovascular ischemia reperfusion injury. Collectively, TRPCs could become a group of drug targets with important physiological functions for the therapy of human cardio/cerebro-vascular diseases.

Despite advances in antithrombotic therapy, the risk of recurrent coronary/cerebrovascular ischemia or venous thromboembolism remains high. Dual pathway antithrombotic blockade, using both antiplatelet and anticoagulant therapy, offers the promise of improved thrombotic protection; however, widespread adoption remains tempered by substantial risk of major bleeding. Here, we report a dual pathway therapeutic capable of site-specific targeting to activated platelets and therapeutic enrichment at the site of thrombus growth to allow reduced dosing without compromised antithrombotic efficacy. We engineered a recombinant fusion protein, SCE5-TAP, which consists of a single-chain antibody (SCE5) that targets and blocks the activated GPIIb/IIIa complex, and tick anticoagulant peptide (TAP), a potent direct inhibitor of activated factor X (FXa). SCE5-TAP demonstrated selective platelet targeting and inhibition of thrombosis in murine models of both carotid artery and inferior vena cava thrombosis, without a significant impact on hemostasis. Selective targeting to activated platelets provides an attractive strategy to achieve high antithrombotic efficacy with reduced risk of bleeding complications.

Brain ischemia, including cerebral ischemia and cerebrovascular ischemia, leads to poor oxygen supply or cerebral hypoxia, and causes brain tissue death or cerebral infarction/ischemic stroke. The troxerutin and cerebroprotein hydrolysate injection (TCHI), is widely applied in China to improve blood supply in ischemic brain tissues and to enhance neuroprotective effects in clinical practice. However, the benefits and detailed underlying mechanism elaborating the effectiveness of TCHI in cerebrovascular diseases require further investigation. Therefore, in the present study, experimental in vivo and in vitro models were employed to investigate the potential mechanisms of TCHI on cerebral ischemic injury. The results demonstrated that TCHI increased the lactate dehydrogenase levels in the brain homogenate and conversely decreased lactic acid levels. TCHI was further observed to significantly increase superoxide dismutase activity and decrease malondialdehyde levels in ischemic brain tissues. In addition, TCHI significantly induced vascular maturation processes, including proliferation, adhesion, migration and tube formation in cultured human umbilical vein endothelial cells. Additionally, TCHI significantly stimulated microvessel formation in the rat aortic ring and chick chorioallantoic membrane assays. Taken together, these results provided strong evidence that TCHI stimulated angiogenesis at multiple steps, and indicated that TCHI attenuated cerebral ischemic damage through the amelioration of oxidative stress and promotion of angiogenesis.

Ethnopharmacological relevance Japanese Angelica acutiloba root (Angelica root) is included in several Kampo medicines including Yokukansan (YKS). Angelica root and YKS are used for the treatment of a variety of psychological and neurodegenerative disorders. Development of safe and effective therapeutic agents against cerebrovascular disorders will improve the treatment of patients with dementia. Aim of the study The effect of Angelica root and YKS on ischemia-impaired memory has not yet been fully investigated. The present study investigated whether Angelica root is also involved in memory improving and neuroprotective effect of YKS in a model of cerebrovascular ischemia. Materials and methods Male Wistar rats grouped into sham rats received saline, and other three groups subjected to repeated cerebral ischemia induced by 4-vessel occlusion (4-VO), received a 7-day oral administration of either saline, Angelica root or YKS. Memory was evaluated by eight-arm radial maze task. Acetylcholine release (ACh) in the dorsal hippocampus was investigated by microdialysis-HPLC. Apoptosis was determined by terminal deoxynucleotidyl transferase (TdT)-mediated fluorescein-deoxyuridine triphosphate (dUTP) nick-end labeling. Results Ischemia induced apoptosis, reduced release of ACh, and impaired the memory (increased error choices and decreased correct choices). Angelica root and YKS improved the memory deficits, upregulated the release of ACh and prevented 4-VO-induced hippocampal apoptosis. Conclusion The dual ACh-increasing and neuroprotective effect of Angelica root could make it a promising therapeutic agent useful for the treatment of symptoms of cerebrovascular dementia. Angelica root could be one of the components contributing to the memory-improving and neuroprotective effects of YKS.

Background Previous meta‐analyses on meat intake and risk of stroke did not report the effect of white meat (poultry meat, excluding fish) and did not examine stroke incidence and mortality separately. We aimed to investigate the relationship of total (red and processed meat), red (unprocessed or fresh red meat), and processed (processed red meat) consumption along with white meat on risk of stroke incidence and mortality. Methods and Results Articles were identified from databases and reference lists of relevant studies up to October 28, 2016. We selected prospective cohort studies on meat consumption specified by types of meat and stroke incidence and mortality reporting relative risks and 95% confidence intervals. The pooled relative risk was estimated using the random‐effects model. Based on the inclusion criteria, 10 articles containing 15 studies (5 articles with 7 studies including 9522 cases of stroke incidence and 254 742 participants and 5 articles with 8 studies containing 12 999 cases of stroke mortality and 487 150 participants) were selected for quantitative synthesis. The pooled relative risks (95% confidence intervals) for total, red, processed and white meat consumption and total stroke incidence were 1.18 (1.09–1.28), 1.11 (1.03–1.20), 1.17 (1.08–1.25), and 0.87 (0.78–0.97), respectively. Total meat consumption (0.97 [0.85–1.11]) and red meat consumption 0.87 (0.64–1.18) were not significantly associated with stroke‐related death. Conclusions The relationship between meat intake and risk of stroke may differ by type of meat. Recommendations for replacing proportions of red and processed meats to white meat for the prevention of stroke may be considered in clinical practice.

[EN] This work presents the advance to development of an algorithm for automatic detection of demyelinating lesions and cerebral ischemia through magnetic resonance images, which have contributed in paramount importance in the diagnosis of brain diseases. The sequences of images to be used are T1, T2, and FLAIR. Brain demyelination lesions occur due to damage of the myelin layer of nerve fibers; and therefore this deterioration is the cause of serious pathologies such as multiple sclerosis (MS), leukodystrophy, disseminated acute encephalomyelitis. Cerebral or cerebrovascular ischemia is the interruption of the blood supply to the brain, thus interrupting; the flow of oxygen and nutrients needed to maintain the functioning of brain cells. The algorithm allows the differentiation between these lesions., The authors are grateful with the Universidad Técnica Particular de Loja Hospital (H-UTPL) for collaborate with the data for this project.

We believe Meniere attacks arise as a chance association of endolymphatic hydrops and vascular risk factors for intracerebral ischemia. Hydrops acts as a variable Starling resistor upon the inner ear vasculature that is capable of inducing ischemic attacks only in people with reduced perfusion pressure in the ear. The unique characteristics of the attacks (loss of vestibular response and hearing acutely followed by a return to apparent normalcy over hours) are explained by the differential sensitivity of the inner ear tissues to transient ischemia, with the sensory tissues (dendrites, hair cells) vulnerable to hours-long ischemia/reperfusion injury, and the stria vulnerable to ischemia due to its high metabolic rate. Permanent hearing loss and vestibular damage after many attacks would result when small areas of irreversible sensory cell damage accumulate and become confluent. This theory is supported by the strong correlation of hydrops with Meniere attacks, the finding that autoregulation of cochlear blood flow is impaired in the hydropic ear, and studies demonstrating that symptoms and signs in people and in animal models vary with conditions that alter perfusion pressure in the inner ear. Induction of Meniere attacks in animal models requires both hydrops and a mechanism that reduces perfusion pressure, such as epinephrine injection or head dependency. There is a strong clinical association between Meniere attacks and disorders that increase the risk for cerebrovascular ischemia, such as migraine. The excitable tissues in the sensory structures have long been known to be more vulnerable to ischemia than the remaining aural tissues, and are now known to be vulnerable to excitotoxicity induced by ischemia/reperfusion. This correlates well with autopsy evidence of damage to dendrites and hair cells and with strial atrophy in late Meniere disease cases. If this hypothesis is confirmed, treatment of vascular risk factors may allow control of symptoms and result in a decreased need for ablative procedures in this disorder. If attacks are controlled, the previously inevitable progression to severe hearing loss may be preventable in some cases.

Although the clinical features in some patients with cerebrovascular ischemia may be ill defined, majority of the patients present with focal neurological deficits caused by an arterial occlusion, and the clinical presentations are usually referable to the involved arterial territory. Therefore, vascular imaging constitutes an important component of the diagnostic workup. Cervical duplex ultrasonography of carotid and vertebral arteries is employed to evaluate the extracranial vasculature while transcranial Doppler provides important information about intracranial hemodynamic changes in cerebrovascular ischemia. These two components of cerebrovascular ultrasonography are fast and reproducible, and can be performed at the bedside. They provide real-time information about the status of cervico-cranial arterial patency and various hemodynamic alterations, including collateral flow. The information obtained from cerebrovascular ultrasonography is useful for diagnostic as well as prognostic purposes. Furthermore, it can be used to monitor cerebral blood flow for extended periods and aid in decision making for various interventions. The hemodynamic information obtained from cerebrovascular ultrasonography helps in determining the underlying mechanisms of brain ischemia, and is complementary to the clinical examination and other imaging modalities.We describe the technique of performing cervical duplex sonography, diagnostic criteria for arterial stenosis, characterizing plaque morphology, measuring intima-media thickness and various pitfalls while performing the test.

Takayasu's arteritis (TA) is a rare, idiopathic, chronic inflammatory disease associated with cell-mediated inflammation and involving predominantly the aorta and its primary branches. TA results in stenosis, occlusion or aneurysmal degeneration of large arteries pathologically. However, the incidence of dissection in arteries is low. As one of the primary causes of aortic dissection-associated ischemic stroke in young adults, only a limited number of TA cases presenting with aortic dissection have been published to date. In the present study, a case of common carotid artery dissection in a young patient with TA, without evident clinical manifestations, is presented. This is a rare clinical phenomenon, but may be a risk factor of acute cerebrovascular events. Clinical examination and satisfactory imaging are crucial for the correct diagnosis and management of patients with TA with dissection in arteries, and great attention is required in order to prevent the occurrence of cerebrovascular ischemia.

BACKGROUND AND PURPOSE: Cerebral thermoregulation remains poorly understood. Temperature dysregulation is deeply implicated in the potentiation of cerebrovascular ischemia. We present a multiphasic, MR thermographic study in a nonhuman primate model of MCA infarction, hypothesizing detectable brain temperature disturbances and brain-systemic temperature decoupling. MATERIALS AND METHODS: Three Rhesus Macaque nonhuman primates were sourced for 3-phase MR imaging: 1) baseline MR imaging, 2) 7-hour continuous MR imaging following minimally invasive, endovascular MCA stroke induction, and 3) poststroke day 1 MR imaging follow-up. MR thermometry was achieved by multivoxel spectroscopy (semi-localization by adiabatic selective refocusing) by using the proton resonance frequency chemical shift. The relationship of brain and systemic temperatures with time and infarction volumes was characterized by using a mixed-effects model. RESULTS: Following MCA infarction, progressive cerebral hyperthermia was observed in all 3 subjects, significantly outpacing systemic temperature fluctuations. Highly significant associations were observed for systemic, hemispheric, and global brain temperatures (F-statistic, P = .0005 for all regressions) relative to the time from stroke induction. Significant differences in the relationship between temperature and time following stroke onset were detected when comparing systemic temperatures with ipsilateral (P = .007), contralateral (P = .004), and infarction core (P = .003) temperatures following multiple-comparisons correction. Significant associations were observed between infarction volumes and both systemic (P ≤ .01) and ipsilateral (P = .04) brain temperatures, but not contralateral brain temperature (P = .08). CONCLUSIONS: Successful physiologic and continuous postischemic cerebral MR thermography was conducted and prescribed in a nonhuman primate infarction model to facilitate translatability. The results confirm hypothesized temperature disturbance and decoupling of physiologic brain-systemic temperature gradients. These findings inform a developing paradigm of brain thermoregulation and the applicability of brain temperature as a neuroimaging biomarker in CNS injury.

The hippocampal formation is one of the brain regions most sensitive to ischemic damage. However, there are no studies about changes in hippocampal neuronal activity during and after a selective unilateral hippocampal ischemia. We developed a novel unilateral cerebrovascular ischemia model in mice that selectively shuts down blood supply to the ipsilateral hippocampal formation. Using a modified version of the photothrombotic method, we stereotaxically targeted the initial ascending part of the longitudinal hippocampal artery in urethane anesthetized and rose bengal-injected mice. To block blood flow in the targeted artery, we photoactivated the rose bengal by illuminating the longitudinal hippocampal artery through an optical fiber inserted into the brain.In vivofield potential recordings in the CA1 region of the hippocampus before, during and after the induction of ischemia demonstrated a high-frequency discharge (HFD) reaching frequencies of >300 Hz and lasting 7–24 s during the illumination consistent with a massive synchronous neuronal activity. The HFD was invariably followed by a DC voltage shift and a decreased activity at both low (30–57 Hz)- and high (63–119 Hz)-gamma frequencies. This decrease in gamma activity lasted for the entire duration of the recordings (∼160 min) following ischemia. The contralateral hippocampus displayed HFDs but with different frequency spectra and without DC voltage shifts or long-lasting decreases in gamma oscillations. Our findings reveal for the first time the acute effects of unilateral hippocampal ischemia on ensemble hippocampal neuronal activities.

In children with sickle cell disease (SCD), adenotonsillar hypertrophy or recurrent tonsillitis are frequently linked with an increased risk of obstructive sleep apnea, cerebrovascular ischemia, or frequent pain episodes and often require an adenoidectomy and/or tonsillectomy. Interventions designed to prevent these complications, control vaso-occlusive pain episodes, and avoid hospitalizations may reduce the significant personal and economic burden of SCD. This study compares episode recurrence and treatment costs for cerebrovascular ischemia, vaso-occlusive pain, acute chest syndrome (ACS), and obstructive sleep apnea in children who had an adenotonsillectomy (A/T surgery, N = 256; 11.7%) and a matched cohort of those who did not (N = 512; 23.3%) from a cohort of 2,194 children and adolescents with SCD from South Carolina's Medicaid system. A/T surgery was associated with a significantly reduced rate of visits over time for obstructive sleep apnea and cerebrovascular ischemia (e.g., stroke, transient ischemic attacks), but not with any change in the rate of visits for vaso-occlusive pain or ACS/pneumonia visits. The rate of mean acute (emergency and inpatient) service costs was significantly decreasing over time after an increase about the time the A/T surgery was performed. The cost-effectiveness of adenoidectomy and/or tonsillectomy for treating obstructive sleep apnea and preventing cerebrovascular ischemia without increasing vaso-occlusive pain episodes or long-term acute service costs in routine clinical practice settings was demonstrated. The matched control group of SCD patients without A/T surgery contained more patients with severe vaso-occlusive pain episodes, ACS visits, and higher mean total costs over time and appears to represent a different phenotype of children with SCD.

Heparin-induced thrombocytopenia (HIT) is caused by platelet-activating antiplatelet factor 4/heparin antibodies. However, clinical HIT (thrombocytopenia or thrombosis, or both) develops in only a minority of patients who form antibodies. It is difficult to distinguish HIT from non-HIT thrombocytopenia in patients after ventricular assist device (VAD) implantation. Further, the risks of heparin-induced immunization and clinical HIT approach 65% and 10%, respectively, in this patient population, with a particularly high risk of cerebrovascular ischemia/infarction. Given the apparent high risk of HIT and its complications, and the diagnostic challenges, we suggest that the VAD patient population be evaluated using alternative, nonheparin agents for routine postimplantation anticoagulation.

Background Changes in cerebral perfusion are an important feature of the pathophysiology of sickle cell anemia (SCA); cerebrovascular ischemia occurs frequently and leads to neurocognitive deficits, silent infarcts, and overt stroke. Non-invasive MRI methods to measure cerebral blood flow (CBF) by arterial spin labeling (ASL) afford new opportunities to characterize disease- and therapy-induced changes in cerebral hemodynamics in patients with SCA. Recent studies have documented elevated gray matter (GM) CBF in untreated children with SCA, but no measurements of white matter (WM) CBF have been reported. Procedures Pulsed ASL with automated brain image segmentation-classification techniques were used to determine the CBF in GM, WM, and abnormal white matter (ABWM) of 21 children with SCA, 18 of whom were receiving hydroxyurea therapy. Results GM and WM CBF were highly associated (R2 = 0.76, P

Background: Carotid intima-media thickness (IMT) is increasingly identified as a marker of atherosclerosis and increased risk of cerebrovascular disease. Aim: We aimed to investigate the prevalence of carotid IMT in asymptomatic Indian individuals, more than 40 years of age, and correlate it with other risk factors for cerebrovascular ischemia. Materials and Methods: Individuals attending outpatient services of Nizam′s Institute of Medical Sciences, who were asymptomatic for cerebrovascular ischemia underwent detailed history and carotid Doppler examination. IMT on mid common carotid artery (CCA) was measured. All subjects′ blood was taken for biochemical estimation of fasting blood sugar and total cholesterol levels. Results: Out of 1,392 subjects, 571 (41%) had abnormal IMT and 821 (59%) had normal IMT. On comparison of the two groups, the factors significantly associated with abnormal IMT were mean older age (59 vs 50.7 years; P < 0.0001) and higher prevalence of hypertension (257 (45%) vs 236 (28.7%); P < 0.0001), diabetes (159 (27.8%) vs 139 (16.9%); P < 0.0001), and hypercholesterolemia (124 (21.7%) vs113 (13.7%); P = 0.0001). After adjustment with multiple logistic regression, significant predictors were age (odds 3.2; 95% confidence interval (CI) 2.5-4.1), male gender (odds 1.5; 95% CI 1.1-1.9), hypercholesterolemia (odds 1.5; 95% CI 1.1-2.0), hypertension (odds 1.4; 95% CI 1.1-1.8), and diabetes (odds 1.3; 95% CI 1.0-1.7). Conclusion: We found age, sex, hypertension, diabetes, and hypercholesterolemia to be independent risk factor for abnormal IMT in asymptomatic subjects over 40 years of age.

Purpose Takayasu arteritis is an indication for bypass surgery when this condition results in severe cerebrovascular ischemia due to occlusion of the carotid arteries. We reviewed the patients with Takayasu arteritis who received aorto-carotid bypass due to cerebrovascular ischemia. Methods A retrospective review was performed on 19 patients with Takayasu arteritis who underwent aorto-carotid bypass from March 2002 to April 2015. Results All patients were female and the mean of their age was 40.6 ± 15.3 years. Eleven patients (57.9%) underwent aorto-uni-carotid bypass and 8 patients (42.1%) underwent aorto-bi-carotid bypass. Five patients (26.3%) whose postoperative blood pressure was not controlled suffered an intracranial hemorrhage within 8 days after bypass surgery. Of the patients with an intracranial hemorrhage, 2 patients (10.5%) expired on 26 days and 7 years after surgery, and 3 patients (15.8%) resolved spontaneously. One patient (5.3%) expired due to an intracranial infarction 9 years after bypass surgery. The intracranial ischemic symptoms resolved after bypass surgery in all of the surviving patients. None of the patients experienced anastomosis site complication postoperatively. Conclusion Aorto-carotid bypass is effective for treating Takayasu arteritis with cerebrovascular ischemia, and the results suggest that postoperative blood pressure should be strictly managed to prevent intracranial hemorrhage.

Objective The purpose of this case report is to describe a patient who presented to a chiropractic physician for evaluation and treatment of neck pain and headache. Clinical features A 45-year-old otherwise healthy female presented for evaluation and treatment of neck pain and headache. Within minutes, non-specific musculoskeletal symptoms progressed to neurological deficits, including limb ataxia and cognitive disturbances. Suspicion was raised for cerebrovascular ischemia and emergent referral was initiated. Intervention and outcome Paramedics were immediately summoned and the patient was transported to a local hospital with a working diagnosis of acute cerebrovascular ischemia. Multiplanar computed tomographic and magnetic resonance imaging with contrast revealed vertebral artery dissection of the V 2 segment in the right vertebral artery. Anticoagulation therapy was administered and the patient was discharged without complications after 5 days in the hospital. Conclusion This case highlights the potential for patients with vertebral artery dissection to present with nonspecific musculoskeletal complaints. Neurological symptoms may not manifest initially, but their sudden onset indicates the possibility of an ischemic cerebrovascular event. We suggest that early recognition and emergent referral for this patient avoided potential exacerbation of an evolving pre-existing condition and resulted in timely anticoagulation treatment.

Hereditary hemorrhagic telangiectasia (HHT), previously known as Osler–Weber–Rendu syndrome, is an autosomal dominant vascular disorder with a variety of clinical manifestations. Mucocutaneous telangiectasias are characteristic of the entity, producing epistaxis and gastrointestinal bleeding that often result in an iron-deficiency anemia. However, life-threatening conditions such as hemorrhage or stroke are usually attributable to the presence of arteriovenous malformations (AVMs) in the pulmonary, cerebral, or hepatic circulations. Pulmonary arteriovenous malformations (PAVMs) are direct communications between the pulmonary arteries and pulmonary veins without an interposed capillary bed; PAVMs thereby serve as a potential conduit for paradoxical embolism that can cause cerebrovascular ischemia or cerebral abscess formation. Also, because PAVMs serve as a physiologic right-to-left shunt, patients can present with high-output heart failure, dyspnea, platypnea, and/or secondary polycythemia. Finally, the friability of the abnormal vasculature often causes PAVMs to increase in size over time or hemorrhage, resulting in hemoptysis or hemothorax. The technical complexity of PAVM embolotherapy and the clinical depth needed to adequately provide long-term follow-up care for the proband and their affected family members makes PAVM management of HHT patients an especially rewarding aspect of clinical interventional radiology.

Cerebrovascular diseases cause brain degeneration and subsequent decline of cognitive functions. In this study, comprehensive magnetic resonance imaging approaches with both structural and blood flow imaging were used to characterize the white matter hyperintensity in the brain, cerebral blood flow, and obstruction of vertebral artery caused by stenosis in various cases of individuals with cerebral vascular and cardiovascular risks. It is demonstrated that vertebral artery stenosis characterized as vertebral artery narrowing and/or reduced blood flow velocity by MRI may be associated with the regional specific cerebral vascular comorbidities detected as white matter hyperintensity and reduction of cerebral blood flow. More specifically, unilateral vertebral artery stenosis led to asymmetric periventricular WMHs, while bilateral vertebral artery with lower blood flow led to symmetric periventricular WMHs. The comprehensive MRI protocol with functional and high resolution structural imaging sequences is capable of providing valuable information on blood flow supply in the vertebral artery and cerebrovascular ischemia in individuals having vertebral and cardiovascular abnormalities.

To the Editor: Vernieri and colleagues1 concluded in their recent article that treatment options in internal carotid artery occlusion can be differentiated on the basis of cerebral hemodynamic status. Specifically, their results has demonstrated that the breath-holding index (BHI) in the middle cerebral artery detected by transcranial Doppler ultrasonography (TCD) is predictive of cerebrovascular ischemic symptoms ipsilateral to the internal carotid artery occlusion. Finally, the authors suggest the use of BHI in selecting patients for the classic or a new type of surgical extracranial/intracranial bypass study. I would like to raise the following comments. First, “carotid stump syndrome” is a well-known phenomenon: continual episodes of transient ischemic attack (TIA) and/or stroke ipsilateral to an occluded internal carotid artery; embolism has been implicated in the pathogenesis, and border-zone infarction is less common.2 3 The source of emboli includes the ipsilateral internal carotid artery stump, the ipsilateral external carotid artery, the contralateral internal and external carotid arteries, the vertebrobasilar system, and the heart. In the study by Vernieri and colleagues,1 patients with significant stenosis of the contralateral carotid artery system, significant vertebral artery disease, or cardiac source of emboli were excluded. These exclusions might have resulted in a lower rate of ischemic stroke, especially on the side contralateral to the carotid artery occlusion, and augmented the importance of hemodynamic mechanisms in producing cerebrovascular ischemia. In addition, I am interested in knowing whether there was any significant stenosis in the external carotid artery ipsilateral to the internal carotid artery occlusion. Second, CT or MRI of the brain was performed at baseline in all the patients with internal carotid artery occlusion, but the neuroimaging findings were not described in the article.1 This information may be important because some “asymptomatic” patients and some symptomatic patients with “TIA only” could have “silent” …

Papillary fibroelastomas are uncommon benign tumors usually involving the heart valves, which historically have been diagnosed at autopsy. With the advent of echocardiography, however, the number of patients diagnosed in life has increased. Papillary fibroelastomas represent a surgically treatable cause of cerebrovascular and cardiovascular ischemia and infarction making their identification clinically important. We report three unusual cases of papillary fibroelastoma; two patients presenting with symptoms of cerebrovascular ischemia and one presenting with myocardial infarction. We also present a comprehensive review of the literature and provide a compilation of all case reports to date.

Patients with systemic lupus erythematosus (SLE) can experience acute neurological events such as seizures, cerebrovascular accidents, and delirium, psychiatric conditions including depression, anxiety, and psychosis, as well as memory loss and general cognitive decline. Neuropsychiatric SLE (NPSLE) occurs in between 30 and 40% of SLE patients, can constitute the initial patient presentation, and may occur outside the greater context of an SLE flare. Current efforts to elucidate the mechanistic underpinnings of NPSLE are focused on several different and potentially complementary pathways, including thrombosis, brain autoreactive antibodies, and complement deposition. Furthermore, significant effort is dedicated to understanding the contribution of neuroinflammation induced by TNF, IL-1, IL-6, and IFN-γ. More recent studies have pointed to a possible role for the TNF family ligand TWEAK in the pathogenesis of neuropsychiatric disease in human lupus patients, and in a murine model of this disease. The blood brain barrier (BBB) consists of tight junctions between endothelial cells (ECs) and astrocytic projections which regulate paracellular and transcellular flow into the central nervous system (CNS), respectively. Given the privileged environment of the CNS, an important question is whether and how the integrity of the BBB is compromised in NPSLE, and its potential pathogenic role. Evidence of BBB violation in NPSLE includes changes in the albumin quotient (Q alb) between plasma and cerebrospinal fluid, activation of brain ECs, and magnetic resonance imaging. This review summarizes the evidence implicating BBB damage as an important component in NPSLE development, occurring via damage to barrier integrity by environmental triggers such as infection and stress; cerebrovascular ischemia as result of a generally prothrombotic state; and immune mediated EC activation, mediated by antibodies and/or inflammatory cytokines. Additionally, new evidence supporting the role of TWEAK/Fn14 signaling in compromising the integrity of the BBB in lupus will be presented.

Relevance of Platelet Functional Disorders in Health and Disease Molecular platelet disorders cause bleeding syndromes of varying severity, best characterized for cell-surface receptor defects involving αIIbβ3 and the GPIb-IX-V complex, and less frequently known to involve distinct signaling pathways or defects of granule formation.1 By contrast, there is a paucity of information on the molecular etiology of the “prothrombotic” platelet, despite long-standing evidence for the role of activated platelets in the development of focal ischemia.2,3 The latter observation is clearly supported by clinical studies of platelet activation markers during transitory and thrombotic vascular events.4–10 Causal evidence for the critical influence of platelets in human vascular events is highlighted by the efficacy of antiplatelet agents as therapeutic and prophylactic modalities in the setting of cerebrovascular ischemia,11–13 as established by observations of fewer nonfatal strokes in patients with prior stroke or transient ischemic attack, and fewer nonfatal strokes among patients treated for completed stroke.14,15 Comparable cardiovascular data exist demonstrating that interventions with antiplatelet agents offer therapeutic efficacy as interventional strategies for coronary artery disease (CAD), acute coronary syndromes, and percutaneous transluminal coronary angioplasty, either in acute settings or as prophylactic modalities.4–7,11,16,17 Antiplatelet agents, however, are not without toxicity, and “breakthrough” thromboembolic episodes remain prevalent.18 Thus the development of risk stratification strategies and/or platelet phenotypic/genotypic assays (“biomarkers”) able to predict responsiveness or adverse events have emerged as a research direction of the biopharmaceutical industry, and have the potential for widespread clinical application.

Background and Purpose Currently, recent infection (primarily bacterial infection) is discussed as a risk factor for cerebrovascular ischemia. The aim of this study was to investigate whether the association of ischemic stroke with recent infection is restricted to stroke subtypes and whether recent infection influences the severity of the postischemic deficit; we also aimed to define biochemical pathways linking infection and ischemic stroke. Methods Analyzing the data of a prospective case-control study, we classified the etiology of cerebrovascular ischemia on the basis of clinical, neuroradiological, sonographical, cardiological, and biochemical data in 159 patients without and in 38 patients with infection within 1 week before ischemia. We assessed the severity of neurological deficits using the Scandinavian Stroke Scale. Results In patients with recent infection compared with patients without infection, the neurological deficit on admission was more severe (median of scores, 41 versus 30.5; P P P P P =.05). Serum levels of C-reactive protein were higher in patients with (20.7±26.8 mg/L) than in those without infection (9.2±23.7 mg/L; P Conclusions Recent infection may be associated with a more severe postischemic deficit and with an increased risk of stroke from cardioembolic origin and from cervical arterial dissection.

É apresentada avaliação crítica da importância da hemorreologia no estabelecimento da conduta terapêutica clínica na insuficiência cerebrovascular aguda. Com essa finalidade são revistos aspectos relativos a fluxo sanguíneo cerebral, insuficiência cerebrovascular e hemorreologia clínica. Em função desses aspectos são avaliados alguns dos principais medicamentos utilizados no presente no tratamento do acidente vascular cerebral e são discutidas normas gerais para prevenção e tratamento das isquemias cerebrais.

Background and Purpose Previous infection is discussed as a risk factor for ischemic stroke in children and younger adults. We tested the hypothesis that the role of recent infection in cerebrovascular ischemia is not restricted to younger patients and investigated which infections are mainly relevant in this respect. Methods We performed a case-control study with 197 patients aged 18 to 80 years with acute cerebrovascular ischemia and 197 randomly selected control subjects matched for sex, age, and area of residence. Results Infection within 1 week before ictus or examination was significantly more common among patients (38 of 197) than control subjects (10 of 197; odds ratio [OR], 4.5; 95% confidence interval [CI], 2.1 to 9.7). Patients more often had febrile and subfebrile infections (≥37.5°C) than control subjects (29 of 197 versus 5 of 197; OR, 7.0; 95% CI, 2.5 to 20). Respiratory tract infections were most common in both groups. Bacterial infections dominated among patients but not among control subjects. Infection increased the risk for cerebrovascular ischemia in all age groups; this reached significance for patients aged 51 to 60 and 61 to 70 years. The profile of vascular risk factors was similar in patients with and patients without previous infection. Infection remained a significant risk factor when previous stroke, hypertension, diabetes mellitus, coronary heart disease, and current smoking were included as covariates in a logistic model (OR, 4.6; 95% CI, 1.9 to 11.3). Conclusions Recent infection, primarily of bacterial origin, may be a risk factor for cerebrovascular ischemia in older as well as younger patients.