Search

Khaled Z Alawneh,1 Liqaa A Raffee,2 Musa Ahmed Mohammed Alshehabat,3 Hazem Haddad,4 Saied A Jaradat5 1Department of Diagnostic Radiology and Nuclear Medicine, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan; 2Department of Accident and Emergency Medicine, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan; 3Department of Clinical Veterinary Medical Sciences, Faculty of Veterinary Medicine, Jordan University of Science and Technology, Irbid, Jordan; 4Haya Biotechnology Center, Jordan University of Science and Technology, Irbid, 22110, Jordan; 5Princess Haya Biotechnology Center, Jordan University of Science and Technology, Irbid, 22110, JordanCorrespondence: Liqaa A RaffeeDepartment of Accident and Emergency Medicine, Faculty of Medicine, Jordan University of Science and Technology, Irbid, JordanEmail laraffee5@just.edu.joPurpose: Ischemic stroke of the brain is still considered one of the most common causes of disability and death in developed and developing countries in human beings despite advances in medicine and technology. This study was conducted to characterize and profile tens of induced biomarkers (microRNAs) after experimentally inducing regional ischemic stroke of the brain by occluding the middle cerebral artery under fluoroscopic guidance using an autologous blood clot.Patient and Methods: A total of six healthy dogs were recruited for this study. The microRNAs were profiled in the blood and urine before and after occluding the middle cerebral artery using genetic techniques.Results: The very highly expressed genes were comprised within cluster A, followed by cluster D in both 24 and 48-hour brain samples. Clusters B and C revealed down-regulated genes, while miRNAs remained up-regulated in the 24-hour samples merely in cluster F. Upregulated genes at 48 hours of reperfusion were included in cluster E. On the other hand, changes were observed after a day on the cluster G genes. Exclusive upregulation was notified after 2 days due to the changes in mIR-138. The normalized gene expression in the test sample is witnessed through Fold-Change, which divides the control sample’s normalized gene expression. Moreover, fold-change has emerged as a significant approach for representing fold-regulation.Conclusion: The microRNAs expression in blood and urine may have a potential role in the diagnosis, prognosis, and assessment of therapy associated with cerebral artery occlusion under fluoroscopic guidance.Keywords: dogs, fluoroscopic induced ischemic brain, microRNAs, middle cerebral artery stroke

Background This study aimed to assess the added value and current applications of SWI in the diagnosis of pediatric non-neoplastic neurological diseases, including its ability to characterize hemorrhage in various brain lesions and its important role in the evaluation of both arterial as well as venous ischemic brain lesions. Results Forty pediatric patients with a median age of 9 years were included in our prospective study; 23 were males and 17 females. SWI had a significantly higher detection rate than conventional MRI for traumatic brain injury (TBI) lesions, hemorrhagic lesions in acute necrotizing encephalopathy (ANEC), and cavernoma lesions (p = 0.005, p = 0.038, and p = 0.046, respectively). The sensitivity, specificity and accuracy of SWI for the detection of venous ischemic insult was 88.9%, 50%, and 76.9% respectively. SWI was significantly better than the conventional MRI (p = 0.046) for the detection of chronic ischemic brain insults and ischemic lesions with added hemorrhagic components. Conclusion SWI is a technique with reasonable acquisition time that could improve the diagnostic performance of MRI for the evaluation of various pediatric non-neoplastic neurological diseases.

Метою дослідження було обґрунтування ефективності церебропротекторної терапії шляхом застосування холіну альфосцерату при ішемічному інсульті. Було проведено обстеження й лікування 25 хворих на ішемічний інсульт. Встановлено, що нейронспецифічна єнолаза є маркером тяжкості нейродеструктивних процесів в ішемізованому головному мозку, а також ефективності терапії. Встановлено, що холіну альфосцерат (Гліатилін) знижує нейродеструктивні процеси в ішемізованому головному мозку, підтверджує вірогідне зниження рівня нейронспецифічної єнолази. Отримані результати є підґрунтям для включення холіну альфосцерату (Гліатилін) у програму інтенсивної терапії мозкового інсульту як ефективного церебропротектора.

The article presents data on the features of cerebral circulation disorders in dogs of brachycephalic breeds. The anatomical breed prerequisites that overload the small circulatory system and, as a result, increase the state of hypoxia are listed. Data from neurological examinations and laboratory studies of such animals are presented. The effectiveness and expediency of using the drug Mexidol-Vet® in animals of this group have been proved. Recommendations for taking the drug to prevent relapses are given.

Multimodal MR imaging provides valuable information in the management of patients with acute ischemic stroke (AIS), with diagnostic, therapeutic, and prognostic implications. MR imaging plays a critical role in treatment decision making for (1) thrombolytic treatment of AIS patients with unknown symptom-onset and (2) endovascular treatment of patients with large vessel occlusion presenting beyond 6 hours from the symptom onset. MR imaging provides the most accurate information for detection of ischemic brain and is invaluable for differentiating AIS from stroke mimics.

Nowadays, amphetamines constitute the prescription drugs most commonly abused by adolescents and young adults (Berman, O’Neill, Fears et al. 2008). The prevalence of problematic (mainly illegal) use of amphetamines as a stimulant by college students, and here especially before serious examinations, has also been rising. This fact represents a serious public health concern. The patient, aged 19, was awakened from from a long-term coma that had lasted 21 days following an amphetamine overdose and manifested tetraparesis, cortical blindness and deficits in cognitive and emotional processes. After a year of rehabilitation the majority of symptoms had disappeared, but cortical blindness andworking memory deficits remained. In addition, frontal lobe syndrome symptoms appeared. After two years of therapy as a result of immense tiredness caused by all an night wedding reception she started to manifest Charles-Bonnet syndrome. She experienced strange visual sensations such as visual hallucinations and saw various non-existing shapes (coloured blots, patterns and fireworks of vivid colours). She also saw objects (often terrifying) as well as animals (mainly African) and people with deformed faces and long teeth, and persons in African dress with feathers and coral beads in their hair. Her real identity was not remembered by the patient for longer than 2 hours and even then she insisted on being referred to as Shakira. She was given a qEEG examination (in open and closed eyes conditions) and ERPs with the use of auditory stimuli at the period when the hallucinations (to a small degree) still occurred. Studies conducted into the functional neuroimaging of the brain work in milliseconds in the examined patient can explain her symptoms. A comparison of the subject’s ERPs with the grand average of ERPs in healthy controls shows that the N170 and N 250 components are impaired in the subject: the occipital-temporal area of the subject brain shows a strong positivity instead of negativities. This positivity might reflect an enhanced reactivity of neurons in the corresponding area induced by the removal of lateral inhibition from the neurons as a result of local damage.

Stroke is a sudden-onset neurological deficit resulting from focal vascular lesions. This is either due to a clot-induced obstruction of a vessel (ischemic stroke) or a rupture of a vessel causing haemorrhage (hemorrhagic stroke). The appropriate diagnosis of brain stroke aphasic patients is a major public health problem one so important for effective rehabilitation. Here an important role is played by the diagnosis of impaired cognitive processes. The aim of the research was to find the index of impaired cognitive control with the use of ERPs in a patient following an ischemic stroke with aphasia. A male patient, aged 69, after an ischemic brain stroke experienced 4 months previously with resulting naming problem, was admitted to the Reintegrative and Teaching Center of the Polish Neuropsychological Society. In the neuropsychological evaluation three neuropsychological tests were employed: (a) the Boston Naming Test-Polish version, to evaluate the naming and word finding problem; (b) the nonverbal Bell test to ascertain a selective, visuospatial and strategic attentional evaluation; (c) the Digit Memory test to evaluate working memory capabilities; (d) ERPs as a neurophys- iological index of impaired cognitive control. Significant changes were observed in testing. All cognitive functions including naming, non- verbal, visuospatial and strategic attention, along with the digit memory deviate substantially from the norm. The patient obtained a lo wer score, compared to the norm (p

Electroconvulsive therapy (ECT) is an effective treatment for various psychiatric conditions. Although rare, prolonged post-ECT delirium is a serious adverse effect of ECT. Various factors, such as underlying brain pathologies, medications, seizure duration, and type of electrode placements play a role in the development of post-ECT delirium. We report a 56-year-old male suffering from 14-day-long post-ECT delirium associated with substance misuse, pesticide exposure, as well as ischemic brain changes. On the basis of the insights from this case, it may be suggested that all patients should be screened for risk factors associated with ECT-related delirium before ECT and that various parameters, such as electrode placement and medications, should be adjusted accordingly.

The brain's response to ischemic injury is an acute and long-term inflammatory process. This process involves activation of resident cells (mainly microglia, hematogenous macrophages), production of proinflammatory mediators and infiltration of various proinflammatory cells (mainly neutrophils and lymphocytes). These cells play an essential role in ischemic brain tissue by releasing either proinflammatory or anti-inflammatory mediators at different time points. However, the exact pathogenesis of proinflammatory or anti-inflammatory genes in this process has not yet been elucidated. This review aims to investigate the inflammatory process of stroke, especially the role of proinflammatory and anti-inflammatory genes in the pathogenesis of stroke. We also summarize the current clinical trials of drugs that target the inflammatory mechanism for intervention.

Smoking-derived nicotine (N) and oral contraceptives (OC) synergistically exacerbate ischemic brain damage in the females and underlying mechanisms remain elusive. Our published study showed that N toxicity is exacerbated by OC via altered mitochondrial function owing to a defect in the activity of cytochrome c oxidase. Here, we investigated the global metabolomic profile of brains of adolescent female Sprague-Dawley rats exposed to N ± OC. Rats were randomly exposed to saline or N + /−OC for 16–21 days followed by random allocation into two cohorts. One cohort underwent transient middle cerebral artery occlusion and histopathology was performed 30 days later. From the second cohort, cortical tissues were collected for an unbiased global metabolomic profile. Pathway enrichment analysis showed significant decrease in glucose, glucose 6-phosphate and fructose-6-phosphate, along with a significant increase in pyruvate in the N + /−OC exposed groups when compared to saline ( p

The Circle of Willis (CoW) is the most important collateral pathway communicating between the bilateral carotid system and the posterior circulation. Many techniques have been used to investigate the configuration and function of the CoW and their advantages and disadvantages are reviewed here. In previous studies, morphometric variation in CoW has been widely detected; however, the frequency of variation ranges largely, between 10% and 85%. Some differences in reported frequency may reflect differences in: the definition of CoW variation, the methods used to examine variation and study populations. Two conclusions, however, are clear: (i) the prevalence of variation in the posterior circle is higher than in that of the anterior circle; and (ii) variations in the CoW are correlated with cerebral or carotid vessel diseases. Although the cause of the variants remains unclear, both genetic background and hemodynamics could play important roles. Lastly, the correlation between the CoW and ischemic brain diseases is discussed. In future, artificial intelligence will be helpful for evaluating the CoW.

Cardiac arrest (CA) afflicts ~ 550,000 people each year in the USA. A small fraction of CA sufferers survive with a majority of these survivors emerging in a comatose state. Many CA survivors suffer devastating global brain injury with some remaining indefinitely in a comatose state. The pathogenesis of global brain injury secondary to CA is complex. Mechanisms of CA-induced brain injury include ischemia, hypoxia, cytotoxicity, inflammation, and ultimately, irreversible neuronal damage. Due to this complexity, it is critical for clinicians to have access as early as possible to quantitative metrics for diagnosing injury severity, accurately predicting outcome, and informing patient care. Current recommendations involve using multiple modalities including clinical exam, electrophysiology, brain imaging, and molecular biomarkers. This multi-faceted approach is designed to improve prognostication to avoid “self-fulfilling” prophecy and early withdrawal of life-sustaining treatments. Incorporation of emerging dynamic monitoring tools such as diffuse optical technologies may provide improved diagnosis and early prognostication to better inform treatment. Currently, targeted temperature management (TTM) is the leading treatment, with the number of patients needed to treat being ~ 6 in order to improve outcome for one patient. Future avenues of treatment, which may potentially be combined with TTM, include pharmacotherapy, perfusion/oxygenation targets, and pre/postconditioning. In this review, we provide a bench to bedside approach to delineate the pathophysiology, prognostication methods, current targeted therapies, and future directions of research surrounding hypoxic–ischemic brain injury (HIBI) secondary to CA. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s13311-020-00856-z) contains supplementary material, which is available to authorized users.

Ischemic stroke is a destructive vascular disease that carries the risk of high mortality, disability, and eventually the development of full-blown dementia. Despite the continuous development of new prognostic methods, the prediction of ischemic sequelae and early and late prognosis of stroke is still much easier said than to apply in practice. Cell-to-cell communication between neuronal, glial, and vascular cells are essential for normal functioning of the brain, and in cerebral ischemia, this communication is interrupted. New research has demonstrated the important role of exosomes in cell-to-cell communication via microRNA transfer, playing an integral role in multicellular crosstalk. Following a stroke, harmful and/or beneficial microRNAs are released into the circulation, significantly affecting the severity and prognosis of a stroke. This chapter provides an overview of the current literature on the possible harmful and beneficial roles of cargo derived from exosomes in ischemic stroke. A snapshot of experimental evidence for the role of exosome-derived microRNAs in ischemic stroke followed by clinical studies exploring the diagnostic and prognostic potential of exosomes in stroke patients are presented. Finally, the promises and pitfalls along with future directions are discussed.

Histoplasmosis is one of the most common endemic mycoses affecting immunocompromised individuals in the United States and Latin America. Involvement of the central nervous system carries higher mortality rates and worse prognosis, given its resemblance to stroke, vasculitis, and meningitis of other etiologies. The diagnosis is challenging, due to its subtle clinical presentation and the poor sensitivity of the cerebrospinal fluid culture. Herein the authors present a case of a middle-aged man with HIV, who presented with intermittent headaches exacerbated by an oculomotor nerve palsy, concerning for acute stroke. A diagnosis of central nervous system histoplasmosis was made, and his neurological deficits subsided after initiation of treatment. The stroke-like syndrome in this scenario may be secondary to granulomatous vasculitis of small caliber cerebral blood vessels. Histoplasmosis of the central nervous system remains a challenging diagnosis, which requires a high index of suspicion by the clinician for an early institution of therapy in order to improve outcomes.

Background and Purpose: Ischemic brain edema can be measured in computed tomography (CT) using quantitative net water uptake (NWU), a recently established imaging biomarker. NWU determined in follow-up CT after mechanical thrombectomy (MT) has shown to be a strong predictor of functional outcome. However, disruption of the blood–brain barrier after MT may also lead to contrast staining, increasing the density on CT scans, and hence, directly impairing measurements of NWU. The purpose of this study was to determine whether dual-energy dual-layer CT (DDCT) after MT can improve the quantification of NWU by measuring NWU in conventional polychromatic CT images (CP-I) and virtual non-contrast images (VNC-I). We hypothesized that VNC-based NWU (vNWU) differs from NWU in conventional CT (cNWU).Methods: Ten patients with middle cerebral artery occlusion who received a DDCT follow-up scan after MT were included. NWU was quantified in conventional and VNC images as previously published and was compared using paired sample t-tests.Results: The mean cNWU was 3.3% (95%CI: 0–0.41%), and vNWU was 11% (95%CI: 1.3–23.4), which was not statistically different (p = 0.09). Two patients showed significant differences between cNWU and vNWU (Δ = 24% and Δ = 36%), while the agreement of cNWU/vNWU in 8/10 patients was high (difference 2.3%, p = 0.23).Conclusion: NWU may be quantified precisely on conventional CT images, as the underestimation of ischemic edema due to contrast staining was low. However, a proportion of patients after MT might show significant contrast leakage resulting in edema underestimation. Further research is needed to validate these findings and investigate clinical implications.

This case report presents a 36-year old man with a disseminated sporotrichosis who presented with seizures and crusted lesions all over the body. Imaging studies revealed acute ischemic brain event with haemorrhagic transformation in right frontal lobe. Skin biopsy showed Sporothrix schenckii. He was treated with standard amphotericin B. Despite therapy, he developed consciousness loss, multiorgan-failure and eventually expired. Necropsy findings showed renal, hepatic, splenic, prostate, testicles and meningeal/cerebral involvement. Keywords: Necropsy, Brazil, Sporotrichosis, Sporothrix brasiliensis, Sporothrix schenckii, Endemic mycoses

Mannose-binding lectin (MBL), an initiator of the lectin pathway, is detrimental in ischemic stroke. MBL deposition on the ischemic endothelium indicates the beginning of its actions, but downstream mechanisms are not clear yet. We investigated MBL interactions with the ischemic endothelium by exposing human brain microvascular endothelial cells (hBMECs) to protocols of ischemia. Cells were exposed to hypoxia or oxygen–glucose deprivation (OGD), and re-oxygenated with human serum (HS) or recombinant MBL (rhMBL). Hypoxic hBMECs re-oxygenated with HS showed increased complement system activation (C3c deposition, +59%) and MBL deposition (+93%) than normoxic cells. Super-resolution microscopy showed MBL internalization in hypoxic cells and altered cytoskeletal organization, indicating a potential MBL action on the endothelial structure. To isolate MBL effect, hBMECs were re-oxygenated with rhMBL after hypoxia/OGD. In both conditions, MBL reduced viability (hypoxia: −25%, OGD: −34%) compared to conditions without MBL, showing a direct toxic effect. Ischemic cells also showed greater MBL deposition (hypoxia: +143%, OGD: +126%) than normoxic cells. These results were confirmed with primary hBMECs exposed to OGD (increased MBL-induced cell death: +226%, and MBL deposition: +104%). The present findings demonstrate that MBL can exert a direct deleterious effect on ischemic brain endothelial cells in vitro, independently from complement activation.

Futile recanalization with poor clinical outcome after endovascular treatment of acute ischemic stroke is poorly understood. Recently, vessel recanalization has been associated with reduced ischemic brain edema in patients with good clinical outcome. As edema volume (EV) may be quantified in computed tomography (CT), we hypothesized that higher EV after revascularization predicts futile recanalization with poor outcome.In this observational study, 67 ischemic stroke patients with M1 middle cerebral artery occlusion fulfilled all inclusion criteria and were analyzed. All patients received successful endovascular recanalization (thrombolysis in cerebral infarction scale 2b/3) and subsequent follow-up CT 24 hours later. Edema volume within the infarct lesion was calculated in follow-up CT applying lesion water uptake quantification and was used to predict clinical outcome (Modified Rankin Scale [mRS] after 90 days) compared with infarct volume.The median EV after thrombectomy was 1.6 mL (interquartile range, 0.2-4.2 mL) in patients with mRS 0 to 4 and 8.6 mL (interquartile range, 2.0-49.8 mL) in patients with mRS 5 to 6 (P = 0.0008). In regression analysis, an EV increase of 1 mL was associated with an 8.0% increased likelihood of poor outcome (95% confidence interval, 2.8%-15.4%; P = 0.008). Based on univariate receiver operating characteristic curve analysis, absolute EV over 4.2 mL predicted poor outcome (mRS 5-6) with good discriminative power (area under curve, 0.74; 95% confidence interval, 0.62-0.84; specificity, 77%; sensitivity, 68%). In comparison, the area under curve for infarct volume was 0.68.Elevated EV after endovascular thrombectomy was associated with poor clinical outcome and may indicate futile recanalization.

Long noncoding RNAs (lncRNA) expression profiles change in the ischemic brain after stroke, but their roles in specific cell types after stroke have not been studied. We tested the hypothesis that lncRNA modulates brain injury by altering macrophage functions. Using RNA deep sequencing, we identified 73 lncRNAs that were differentially expressed in monocyte-derived macrophages (MoDMs) and microglia-derived macrophages (MiDMs) isolated in the ischemic brain three days after stroke. Among these, the lncRNA, GM15628, is highly expressed in pro-inflammatory MoDMs but not in MiDMs, and are functionally related to its neighbor gene, lymphocyte cytosolic protein 1 (LCP1), which plays a role in maintaining cell shape and cell migration. We termed this lncRNA as Macrophage contained LCP1 related pro-inflammatory lncRNA, Maclpil. Using cultured macrophages polarized by LPS, M(LPS), we found that downregulation of Maclpil in M(LPS) decreased pro-inflammatory gene expression while promoting anti-inflammatory gene expression. Maclpil inhibition also reduced the migration and phagocytosis ability of MoDMs by inhibiting LCP1. Furthermore, adoptive transfer of Maclpil silenced M(LPS), reduced ischemic brain infarction, improved behavioral performance and attenuated penetration of MoDMs in the ischemic hemisphere. We conclude that by blocking macrophage, Maclpil protects against acute ischemic stroke by inhibiting neuroinflammation.

Background: Authors have been advocating the research ideology that a computer-aided diagnosis (CAD) system trained using lots of patient data and physiological signals and images based on adroit integration of advanced signal processing and artificial intelligence (AI)/machine learning techniques in an automated fashion can assist neurologists, neurosurgeons, radiologists, and other medical providers to make better clinical decisions. Summary: This paper presents a state-of-the-art review of research on automated diagnosis of 5 neurological disorders in the past 2 decades using AI techniques: epilepsy, Parkinson’s disease, Alzheimer’s disease, multiple sclerosis, and ischemic brain stroke using physiological signals and images. Recent research articles on different feature extraction methods, dimensionality reduction techniques, feature selection, and classification techniques are reviewed. Key Message: CAD systems using AI and advanced signal processing techniques can assist clinicians in analyzing and interpreting physiological signals and images more effectively.

Melatonin has a role in the cell survival signaling pathways as a candidate for secondary stroke prevention. Therefore, in the present study, the coordination of ipsilateral and contralateral hemispheres to evaluate delayed post-acute effect of melatonin was examined on recovery of the cell survival and apoptosis after stroke. Melatonin was administered (4 mg/kg/day) intraperitoneally for 45 days, starting 3 days after 30 min of middle cerebral artery occlusion. The genes and proteins related to the cell survival and apoptosis were investigated by immunofluorescence, western blotting, and RT-PCR techniques after behavioral experiments. Melatonin produced delayed neurological recovery by improving motor coordination on grip strength and rotarod tests. This neurological recovery was also reflected by high level of NeuN positive cells and low level of TUNEL-positive cells suggesting enhanced neuronal survival and reduced apoptosis at the fifty-fifth day of stroke. The increase of NGF, Nrp1, c-jun; activation of AKT; and dephosphorylation of ERK and INK at the fifty-fifth day showed that cell survival and apoptosis signaling molecules compete to contribute to the remodeling of brain. Furthermore, an increase in the CREB and Atf-1 expressions suggested the melatonin-s strong reformative effect on neuronal regeneration. The contralateral hemisphere was more active at the latter stages of the molecular and functional regeneration which provides a further proof of principle about melatonin-s action on the promotion of brain plasticity and recovery after stroke.

Stroke is one of the leading causes of death and disability worldwide with limited therapeutic options. Melatonin can attenuate ischemic brain damage with improved functional outcomes. However, the cellular mechanisms of melatonin-driven neuroprotection against post-stroke neuronal death remain unknown. Here, distal middle cerebral artery occlusion (dMCAO) was performed in C57BL/6j mice to develop an ischemic stroke in vivo model. Melatonin was injected intraperitoneally immediately after ischemia, and 24 and 48 hours later. Melatonin treatment, with 5 to 20 mg/kg, elicited a dose-dependent decrease in infarct volume and concomitant increase in sensorimotor function. At the molecular level, phosphorylation of PTEN and Akt were increased, whereas PTEN activity was decreased in melatonin treated animals 72 hours after dMCAO. At the cellular level, oxygenglucose deprivation (OGD) challenge of neuronal cell line Neuro-2a (N2a) and primary neurons supported melatonin’s direct protection against neuronal cell death. Melatonin treatment reduced LDH release and neuronal apoptosis at various time points, markedly increased Akt phosphorylation in neuronal membrane, but significantly suppressed it in the cytoplasm of post-OGD neurons. Mechanistically, melatonin-induced Akt phosphorylation and neuronal survival was blocked by Wortmannin, a potent PIP3 inhibitor, exposing increased PI3K/Akt activation as a central player in melatonin-driven neuroprotection. Finally, PTEN knock-down through siRNA significantly inhibited PI3K/Akt activation and cell survival following melatonin treatment, suggesting that melatonin protection against ischemic brain damage, is at least partially, dependent on modulation of the PTEN/PI3K/Akt signaling axis.

KEY POINTS • Computed tomographic perfusion (CTP) is increasingly being used in the characterization of brain ischemia.• Variations in post-processing protocols continue to be a challenge, resulting in a slight variation of CTP results.• We need to adopt a universal acquisition protocol to help optimize output of CTP.

BACKGROUND: The relationship between plaque calcification and new ischemic brain lesions after carotid artery stenting (CAS) remains controversial. The purpose of this study was to determine if the circumferential degree of carotid calcification is associated with new ischemic brain lesions on diffusion-weighted imaging (DWI) after CAS. METHODS: A total of 96 patients with carotid stenosis of ≥50% who underwent CAS were enrolled in the study. All patients underwent preoperative carotid computed tomography (CT), and preoperative and postoperative brain MRI. The brain MRI sequences included T1WI, T2WI, T2-fluid-attenuated inversion recovery (FLAIR), and DWI. The location, circumferential degree, volume, percentage volume, maximum density, mean density, Agatston score of carotid calcification, and total plaque volume were assessed and compared between patients with and without new ischemic brain lesions after CAS. Univariate and multivariate analyses were performed to evaluate predictors of new ischemic brain lesions. RESULTS: All of the 96 patients (67.8±6.8 years of age, 83.3% men) were included in the analysis. New ischemic brain lesions on DWI were observed in 40 patients (41.7%). Patients with new ischemic brain lesions after CAS had a larger circumferential degree of calcification than those without new ischemic brain lesions (P

Current treatment for acute ischemic stroke aims at recanalizing the occluded blood vessel to reperfuse ischemic brain tissue. Clot removal can be achieved pharmacologically with a thrombolytic drug, such as recombinant tissue plasminogen activator, or with mechanical thrombectomy. However, reopening the occluded vessel does not guarantee full tissue reperfusion, which has been referred to as reperfusion failure. When it occurs, reperfusion failure significantly attenuates the beneficial effect of recanalization therapy and severely affects functional recovery of stroke patients. The mechanisms of reperfusion failure are somewhat complex and not fully understood. Briefly, after stroke, capillaries show stalls, constriction and luminal narrowing, being crowded with neutrophils, and fibrin&ndash, platelet deposits. Furthermore, after recanalization in stroke patients, a primary clot can break, dislodge, and occlude distal arterial branches further downstream. In this review, we highlight a rodent model that allows studying the pathophysiological mechanisms underlying reperfusion failure after stroke. We also describe the vascular and intravascular changes involved in reperfusion, which may provide relevant therapeutic targets for improving treatment of stroke patients.

Ischemic stroke is a leading cause for neurologic disability worldwide, for which reperfusion is the only available treatment. Neuroimaging in stroke guides treatment, and therefore determines the clinical outcome. However, there are currently no imaging biomarkers for the status of the ischemic brain tissue. Such biomarkers could potentially be useful for guiding treatment in patients presenting with ischemic stroke. Hyperpolarized 13C MR of [1-13C]pyruvate is a clinically translatable method used to characterize tissue metabolism non-invasively in a relevant timescale. The aim of this study was to utilize hyperpolarized [1-13C]pyruvate to investigate the metabolic consequences of an ischemic insult immediately during reperfusion and upon recovery of the brain tissue. The rates of lactate dehydrogenase (LDH) and pyruvate dehydrogenase (PDH) were quantified by monitoring the rates of [1-13C]lactate and [13C]bicarbonate production from hyperpolarized [1-13C]pyruvate. 31P NMR of the perfused brain slices showed that this system is suitable for studying ischemia and recovery following reperfusion. This was indicated by the levels of the high-energy phosphates (tissue viability) and the chemical shift of the inorganic phosphate signal (tissue pH). Acidification, which was observed during the ischemic insult, has returned to baseline level following reperfusion. The LDH/PDH activity ratio increased following ischemia, from 47.0 ± 12.7 in the control group (n = 6) to 217.4 ± 121.3 in the ischemia-reperfusion group (n = 6). Following the recovery period (ca. 1.5 h), this value had returned to its pre-ischemia (baseline) level, suggesting the LDH/PDH enzyme activity ratio may be used as a potential indicator for the status of the ischemic and recovering brain.

The purpose – to carry out the analysis of the current data concerning relationships inthe “bowels microbiota-brain” system at ischemia-reperfusion damages of the brain.Conclusions.1. The analysis of the literature data testify to the views discrepancy, existing today, on therole of the bowels dysbacteriosis (neuroprotective or neurodegenerative) in the clinicalcourse of ischemic damages of the brain.2. Numerous experimental investigations substantiated the bowels microbiota role:homeostasis derangements of T-cells, which have the determined role in the secondaryneuroinflammation following cerebral ischemia; in the ratio change of their subpopulationsTreg-Th17 and migration of the bowels lymphocytes into the ischemic brain.