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Cerebellar injury in preterm infants with central nervous system (CNS) hemorrhage results in lasting neurological deficits and an increased risk of autism. The impact of blood-induced pathways on cerebellar development remains largely unknown, so no specific treatments have been developed to counteract the harmful effects of blood after neurovascular damage in preterm infants. Here, we show that fibrinogen, a blood-clotting protein, plays a central role in impairing neonatal cerebellar development. Longitudinal MRI of preterm infants revealed that cerebellar bleeds were the most critical factor associated with poor cerebellar growth. Using inflammatory and hemorrhagic mouse models of neonatal cerebellar injury, we found that fibrinogen increased innate immune activation and impeded neurogenesis in the developing cerebellum. Fibrinogen inhibited sonic hedgehog (SHH) signaling, the main mitogenic pathway in cerebellar granule neuron progenitors (CGNPs), and was sufficient to disrupt cerebellar growth. Genetic fibrinogen depletion attenuated neuroinflammation, promoted CGNP proliferation, and preserved normal cerebellar development after neurovascular damage. Our findings suggest that fibrinogen alters the balance of SHH signaling in the neurovascular niche and may serve as a therapeutic target to mitigate developmental brain injury after CNS hemorrhage.

Lisfranc injuries are uncommon but frequently misdiagnosed and carry a high rate of morbidity. This review highlights the pearls and pitfalls of Lisfranc injuries, including presentation, diagnosis, and management in the emergency department (ED) based on current evidence. Lisfranc injuries are caused by high- or low-energy trauma to the tarsometatarsal (TMT) joint complex. The severity of injury exists on a spectrum, ranging from minor subluxations to fractures and dislocations involving the TMT joint complex. They can be complicated by compartment syndrome, neurovascular compromise, and open fractures. Prompt diagnosis is critical in preventing chronic pain and mobility challenges, as even small subluxations can result in significant morbidity. Lisfranc injuries should be considered in all patients with a foot injury. Patients with Lisfranc injuries most commonly present with midfoot pain, swelling, or ecchymosis. Despite the importance of a timely diagnosis, Lisfranc injuries are commonly missed on plain radiographs due to their often subtle findings. When x-rays are negative but there is significant clinical suspicion, emergency clinicians should obtain advanced imaging such as computed tomography to aid in diagnosis. All Lisfranc injuries should be discussed with orthopedic surgery to determine definitive management. Patients who can be discharged should be made non-weightbearing and placed in a short-leg splint. The consideration of Lisfranc injuries can help emergency clinicians make a timely diagnosis to prevent future complications. [ABSTRACT FROM AUTHOR]

Bioassembly encompasses various techniques such as bioprinting, microfluidics, organoids, and self-assembly, enabling advances in tissue engineering and regenerative medicine. Advancements in bioassembly technologies have enabled the precise arrangement and integration of various cell types to more closely mimic the complexity functionality of the neurovascular unit (NVU) and that of other biodiverse multicellular tissue structures. In this context, bioprinting offers the ability to deposit cells in a spatially controlled manner, facilitating the construction of interconnected networks. Scaffold-based assembly strategies provide structural support and guidance cues for cell growth, enabling the formation of complex bio-constructs. Self-assembly approaches utilize the inherent properties of cells to drive the spontaneous organization and interaction of neuronal and vascular components. However, recreating the intricate microarchitecture and functional characteristics of a tissue/organ poses additional challenges. Advancements in bioassembly techniques and materials hold great promise for addressing these challenges. The further refinement of bioprinting technologies, such as improved resolution and the incorporation of multiple cell types, can enhance the accuracy and complexity of the biological constructs; however, developing bioinks that support the growth of cells, viability, and functionality while maintaining compatibility with the bioassembly process remains an unmet need in the field, and further advancements in the design of bioactive and biodegradable scaffolds will aid in controlling cell adhesion, differentiation, and vascularization within the engineered tissue. Additionally, integrating advanced imaging and analytical techniques can provide real-time monitoring and characterization of bioassembly, aiding in quality control and optimization. While challenges remain, ongoing research and technological advancements propel the field forward, paving the way for transformative developments in neurovascular research and tissue engineering. This work provides an overview of the advancements, challenges, and future perspectives in bioassembly for fabricating neurovascular constructs with an add-on focus on bioprinting technologies. [ABSTRACT FROM AUTHOR]

The prevalence of hypertension in non-Hispanic black (BL) individuals is the greatest of any racial/ethnic group. Whereas women generally display lower rates of hypertension than men of the same background, BL women display a similar if not greater burden of hypertension compared with BL men. The risk for cardiovascular disease and related events is also highest in BL individuals. Given the importance of the sympathetic nervous system for the regulation of the cardiovascular system, a growing body of literature has investigated sympathetic function in BL and non-Hispanic white (WH) individuals. Here, we are focused on emerging evidence indicating that sympathetic function may be altered in BL individuals, with particular emphasis on the process by which bursts of muscle sympathetic nerve activity (MSNA) are transduced into vasoconstriction and increases in blood pressure (sympathetic vascular transduction). To synthesize this growing body of literature we discuss sex and race differences in 1) sympathetic outflow, 2) sympathetic vascular transduction, and 3) adrenergic receptor sensitivity. Sex differences are discussed foremost, to set the stage for new data indicating a sex dimorphism in sympathetic regulation in BL individuals. Specifically, we highlight evidence for a potential neurogenic phenotype including greater adiposity-independent sympathetic outflow and enhanced sympathetic vascular transduction in BL men that is not observed in BL women. The implications of these findings for the greater hypertension and cardiovascular disease risk in BL adults are discussed along with areas that require further investigation. [ABSTRACT FROM AUTHOR]

Abstract To investigate neurovascular changes; including macular vascular density (VD), thickness of the ganglion cell layer (GCL) and optic nerve head (ONH) parameters in episodic migraine patients. 80 eyes of 40 episodic migraine patients were recruited. Thirty patients having a dominant side of migraine headache were statistically analyzed (5 male and 25 female; mean age 31.67 ± 9.54 years) and compared to 25 eyes of 25 healthy volunteers (5 male and 20 female; mean age of 34.4 ± 12.11 years, p = 0.361). The posterior segment was imaged with Topcon DRI optical coherence tomography (OCT) (Triton Swept source OCT Topcon, Japan), and OCT angiography (OCTA). Comparing the dominant side of migraine patients to controls we found a significant decrease of the VD in the central zone of the superficial and deep capillary plexus (SCP, p = 0.01; DCP, p = 0.004) and an enlarged foveal avascular zone (FAZ, p = 0.054). The GCL thickness was significantly reduced in the central ring (GCL + p = 0.042, GCL + + p = 0.029), as well as the retinal nerve fiber layer (RNFL) thickness in the temporal quadrant (p = 0.021) and border tissue of Elschnig diameter (BTE, p = 0.035). The duration of migraine showed an inverse correlation with SCP in the nasal quadrant (p = 0.016, r = − 0.445) and with all DCP regions [DCP superior (p = 0.004, r = − 0.519), DCP inferior (p = 0.004, r = − 0.519), DCP nasal (p = 0.006, r = − 0.496), DCP temporal (p = 0.005, r = − 0.508), DCP CSF (p

The human penile and clitoral development begins from a morphologically indifferent genital tubercle. Under the influence of androgen, the genital tubercle forms the penis by forming a tubular urethra within the penile shaft. Without the effect of the androgen, the genital tubercle differentiates into the clitoris, and a lack of formation of the urethra within the clitoris is observed. Even though there are similarities during the development of the glans penis and glans clitoris, the complex canalization occurring along the penile shaft eventually leads to a morphological difference between the penis and clitoris. Based on the morphological differences, the main goal of this study was to define the vascular and neuronal anatomy of the developing penis and clitoris between 8 and 12 weeks of gestation using laser scanning confocal microscopy. Our results demonstrated there is a co‐expression of CD31, which is an endothelial cell marker, and PGP9.5, which is a neuronal marker in the penis where the fusion is actively occurring at the ventral shaft. We also identified a unique anatomical structure for the first time, the clitoral ridge, which is a fetal structure running along the clitoral shaft in the vestibular groove. Contrary to previous anatomical findings which indicate that the neurovascular distribution in the developing penis and clitoris is similar, in this study, laser scanning confocal microscopy enabled us to demonstrate finer differences in the neurovascular anatomy between the penis and clitoris. [ABSTRACT FROM AUTHOR]

Background: Antegrade homodigital neurovascular island flaps (AHIFs) are a heterogeneous group of pedicled flaps used for reconstruction of traumatic digital detipping injuries. While numerous single-center studies have documented their use, there are no large or multicentre studies validating their efficacy, applicability, and functional outcomes. We performed a systematic review of the contemporary literature to establish the safety and functional outcomes of this technique. Methods: Electronic searches were performed using PubMED, Embase, and MEDLINE from inception date to October 2020, with further studies identified from study reference lists and independent searches. Relevant studies reported on complications and functional outcomes of the AHIFs, as used for digital detipping injuries. Data were then extracted and analyzed. Results: Twenty-seven studies published between 1974 and 2019 yielded 744 patients. Four studies provided incomplete epidemiologic data, resulting in a total of 559 patients with 584 digital injuries. Index and middle fingers were most frequently involved. Mean final 2-point discrimination (2-PD) was 4.9 mm static and 5.1 mm dynamic, with dynamic 2-PD reported in 2 studies. Mean total active motion of the digit was 200.3°. Mean time to return to work was 6.7 weeks in 10 studies. Flap survivorship was found to be 99.6% in 23 studies. Cold intolerance was the most common complication at 18%, followed by pain and hypersensitivity. Conclusions: Antegrade homodigital neurovascular island flaps provide a safe and effective method of treating distal finger amputations, yielding satisfactory functional outcomes across all ages. Further studies comparing outcomes between the AHIFs and other reconstructive modalities would be useful. [ABSTRACT FROM AUTHOR]

On behalf of the SNS, we are pleased to present the Abstracts of the Annual Meeting which is held at the Congress Center in Basel, Switzerland, from 6–7 June 2024. In total, 83 abstracts were selected, whereof we include 8 abstracts for the Plenary Sessions, 6 abstracts for the SAYN GemSession, 30 abstracts for Poster flash presentations, and 39 abstracts as ePosters. We congratulate all the presenters on their research work and contributions. [ABSTRACT FROM AUTHOR]

Advanced visualization techniques such as maximum intensity projection (MIP) and volume rendering (VR) are useful for evaluating neurovascular anatomy on CT angiography (CTA) of the brain; however, interference from surrounding osseous anatomy is common. Existing methods for removing bone from CTA images are limited in scope and/or accuracy, particularly at the skull base. We present a new brain CTA bone removal tool, which addresses many of these limitations. A deep convolutional neural network was designed and trained for bone removal using 72 brain CTAs. The model was tested on 15 CTAs from the same data source and 17 CTAs from an independent external dataset. Bone removal accuracy was assessed quantitatively, by comparing automated segmentation results to manual segmentations, and qualitatively by evaluating VR visualization of the carotid siphons compared to an existing method for automated bone removal. Average Dice overlap between automated and manual segmentations from the internal and external test datasets were 0.986 and 0.979 respectively. This was superior compared to a publicly available noncontrast head CT bone removal algorithm which had a Dice overlap of 0.947 (internal dataset) and 0.938 (external dataset). Our algorithm yielded better VR visualization of the carotid siphons than the publicly available bone removal tool in 14 out of 15 CTAs (93%, chi-square statistic of 22.5, p-value of

2023 was an important year for research in traumatic brain injury (TBI), particularly as it concerned interests in neuropathology. After reviewing the literature, we present the advancements that we felt were of particular importance to the neuropathology community. Highlighted are articles that report upon: (1) the first large-cohort assessment for the neuropathology of intimate partner violence, (2) the assessment of chronic traumatic encephalopathy (CTE) in young athletes, (3) the observation of cortical sulcal depth vascular changes in CTE, (4) a proposal for a tau immunohistochemical panel to evaluate complex cases of CTE in the context of multiple tauopathies, (5) the relationship of TBI and/or CTE with TDP-43 pathology, (6) repetitive TBI inducing pathology in C9orf72-transgenic mice, (7) radiologic patterns of head and neck injury following vehicular underbody blast exposure, (8) chronic alterations in brain metal content following repetitive impact TBI, (9) neurovascular unit injury following low-level blast exposure, and finally (10) an assessment of Muhammad Ali’s clinical history leading to the conclusion that he suffered from young-onset, idiopathic Parkinson Disease. We close our writing with in memoriam to Dr. Byron A. Kakulas, a renowned figure in the neuropathology of spinal cord injury who we lost in 2023.

Neurons and glia of the peripheral nervous system are derived from progenitor cell populations, originating from embryonic neural crest. The neural crest and vasculature are intimately associated during embryonic development and in the mature central nervous system, in which they form a neurovascular unit comprised of neurons, glia, pericytes, and vascular endothelial cells that play important roles in health and disease. Our group and others have previously reported that postnatal populations of stem cells originating from glia or Schwann cells possess neural stem cell qualities, including rapid proliferation and differentiation into mature glia and neurons. Bone marrow receives sensory and sympathetic innervation from the peripheral nervous system and is known to contain myelinating and unmyelinating Schwann cells. Herein, we describe a population of neural crest-derived Schwann cells residing in a neurovascular niche of bone marrow in association with nerve fibers. These Schwann cells can be isolated and expanded. They demonstrate plasticity in vitro, generating neural stem cells that exhibit neurogenic potential and form neural networks within the enteric nervous system in vivo following transplantation to the intestine. These cells represent a novel source of autologous neural stem cells for the treatment of neurointestinal disorders.

Introduction: Holter-SRA (Stroke Risk Analysis) is an automated analysis of ECG monitoring for Atrial Fibrillation (AF) detection. The aim of this study was to evaluate the rate of AF in undetermined TIA/Rapidly improving stroke symptoms (RISS) patients. Methods: Prospective study of undetermined TIA/RISS patients who presented to the emergency department. Early vascular studies (angio CT, transthoracic echocardiography and ECG) were performed in emergency department. The Holter-SRA device was placed for 2 h and the patients were classified into: confirmed AF, high risk of AF or low risk of AF. Prolonged ambulatory monitoring (7 days) was carried out every month for patients with a high-risk pattern. The results were evaluated until definitive detection of AF or low-risk pattern. The endpoints were rate of AF and vascular recurrence at 90 days. Results: Over a period of 24 months, 83 undetermined TIA/RISS patients were enrolled. The mean age was 70 ± 10 years and 61% were men. The median ABCD2 score was 4 points (1-7). After 2 h of monitoring in the emergency department, AF was detected in one patient (1.2%), 51 patients with a low-risk pattern and 31 patients (37.3%) showed a high-risk pattern of AF. During the ambulatory monitoring, of the 31 patients high risk pattern patients, AF was diagnosed to 17 cases and of the 51 patients with a low-risk pattern, one case experienced a recurrent vascular due to undetected AF (1.9% false negative). Three patients (3.6%) suffered a vascular recurrence within the first 90 days, before AF diagnosis. Conclusions: In our study, AF was detected in 22.9% of the 83 patients with indeterminate TIA/RISS. Holter-SRA has allowed us to increase the detection of AF, especially those patients with a high-risk pattern in the first 3 months. [ABSTRACT FROM AUTHOR]

Background: In the choroid plexus and pituitary gland, vasculature is known to have a permeable, fenestrated phenotype which allows for the free passage of molecules in contrast to the blood brain barrier observed in the rest of the CNS. The endothelium of these compartments, along with secretory, neural-lineage cells (choroid epithelium and pituitary endocrine cells) have been studied in detail, but less attention has been given to the perivascular mesenchymal cells of these compartments. Methods: The Hic1CreERT2 Rosa26LSL−TdTomato mouse model was used in conjunction with a PdgfraH2B−EGFP mouse model to examine mesenchymal cells, which can be subdivided into Pdgfra+ fibroblasts and Pdgfra− pericytes within the choroid plexus (CP) and pituitary gland (PG), by histological, immunofluorescence staining and single-cell RNA-sequencing analyses. Results: We found that both CP and PG possess substantial populations of distinct Hic1+ mesenchymal cells, including an abundance of Pdgfra+ fibroblasts. Within the pituitary, we identified distinct subpopulations of Hic1+ fibroblasts in the glandular anterior pituitary and the neurosecretory posterior pituitary. We also identified multiple distinct markers of CP, PG, and the meningeal mesenchymal compartment, including alkaline phosphatase, indole-n-methyltransferase and CD34. Conclusions: Novel, distinct subpopulations of mesenchymal cells can be found in permeable vascular interfaces, including the CP, PG, and meninges, and make distinct contributions to both organs through the production of structural proteins, enzymes, transporters, and trophic molecules. [ABSTRACT FROM AUTHOR]

Purpose: We conducted a meta-analysis to determine the effect of hyperoxia on muscle sympathetic nerve activity in healthy individuals and those with cardio-metabolic diseases. Methods: A comprehensive search of electronic databases was performed until August 2022. All study designs (except reviews) were included: population (humans; apparently healthy or with at least one chronic disease); exposures (muscle sympathetic nerve activity during hyperoxia or hyperbaria); comparators (hyperoxia or hyperbaria vs. normoxia); and outcomes (muscle sympathetic nerve activity, heart rate, blood pressure, minute ventilation). Forty-nine studies were ultimately included in the meta-analysis. Results: In healthy individuals, hyperoxia had no effect on sympathetic burst frequency (mean difference [MD] − 1.07 bursts/min; 95% confidence interval [CI] − 2.17, 0.04bursts/min; P = 0.06), burst incidence (MD 0.27 bursts/100 heartbeats [hb]; 95% CI − 2.10, 2.64 bursts/100 hb; P = 0.82), burst amplitude (P = 0.85), or total activity (P = 0.31). In those with chronic diseases, hyperoxia decreased burst frequency (MD − 5.57 bursts/min; 95% CI − 7.48, − 3.67 bursts/min; P < 0.001) and burst incidence (MD − 4.44 bursts/100 hb; 95% CI − 7.94, − 0.94 bursts/100 hb; P = 0.01), but had no effect on burst amplitude (P = 0.36) or total activity (P = 0.90). Our meta-regression analyses identified an inverse relationship between normoxic burst frequency and change in burst frequency with hyperoxia. In both groups, hyperoxia decreased heart rate but had no effect on any measure of blood pressure. Conclusion: Hyperoxia does not change sympathetic activity in healthy humans. Conversely, in those with chronic diseases, hyperoxia decreases sympathetic activity. Regardless of disease status, resting sympathetic burst frequency predicts the degree of change in burst frequency, with larger decreases for those with higher resting activity. [ABSTRACT FROM AUTHOR]

Onboard oxygen-generating systems (OBOGSs) provide increased inspired oxygen (FiO2) to mitigate the risk of neurologic injury in high altitude aviators. OBOGSs can deliver highly variable oxygen concentrations oscillating around a predetermined FiO2 set point, even when the aircraft cabin altitude is relatively stable. Steady-state exposure to 100% FiO2 evokes neurovascular vasoconstriction, diminished cerebral perfusion, and altered electroencephalographic activity. Whether non-steady-state FiO2 exposure leads to similar outcomes is unknown. This study characterized the physiologic responses to steady-state and non-steady-state FiO2 during normobaric and hypobaric environmental pressures emulating cockpit pressures within tactical aircraft. The participants received an indwelling radial arterial catheter while exposed to steady-state or non-steady-state FiO2 levels oscillating ± 15% of prescribed set points in a hypobaric chamber. Steady-state exposure to 21% FiO2 during normobaria produced arterial blood gas values within the anticipated ranges. Exposure to non-steady-state FiO2 led to PaO2 levels higher upon cessation of non-steady-state FiO2 than when measured during steady-state exposure. This pattern was consistent across all FiO2 ranges, at each barometric condition. Prefrontal cortical activation during cognitive testing was lower following exposure to non-steady-state FiO2 >50% and <100% during both normobaria and hypobaria of 494 mmHg. The serum analyte levels (IL-6, IP-10, MCP-1, MDC, IL-15, and VEGF-D) increased 48 h following the exposures. We found non-steady-state FiO2 levels >50% reduced prefrontal cortical brain activation during the cognitive challenge, consistent with an evoked pattern of neurovascular constriction and dilation. [ABSTRACT FROM AUTHOR]

Microglia are strongly implicated in the development and progression of Alzheimer's disease (AD), yet their impact on pathology and lifespan remains unclear. Here we utilize a CSF1R hypomorphic mouse to generate a model of AD that genetically lacks microglia. The resulting microglial-deficient mice exhibit a profound shift from parenchymal amyloid plaques to cerebral amyloid angiopathy (CAA), which is accompanied by numerous transcriptional changes, greatly increased brain calcification and hemorrhages, and premature lethality. Remarkably, a single injection of wild-type microglia into adult mice repopulates the microglial niche and prevents each of these pathological changes. Taken together, these results indicate the protective functions of microglia in reducing CAA, blood-brain barrier dysfunction, and brain calcification. To further understand the clinical implications of these findings, human AD tissue and iPSC-microglia were examined, providing evidence that microglia phagocytose calcium crystals, and this process is impaired by loss of the AD risk gene, TREM2.

Although human pluripotent stem cell (PSC)‐derived brain organoids have enabled researchers to gain insight into human brain development and disease, these organoids contain solely ectodermal cells and are not vascularized as occurs during brain development. Here it is created less complex and more homogenous large neural constructs starting from PSC‐derived neuroprogenitor cells (NPC), by fusing small NPC spheroids into so‐called concentroids. Such concentroids consisted of a pro‐angiogenic core, containing neuronal and outer radial glia cells, surrounded by an astroglia‐dense outer layer. Incorporating PSC‐derived endothelial cells (EC) around and/or in the concentroids promoted vascularization, accompanied by differential outgrowth and differentiation of neuronal and astroglia cells, as well as the development of ectodermal‐derived pericyte‐like mural cells co‐localizing with EC networks. Single nucleus transcriptomic analysis revealed an enhanced neural cell subtype maturation and diversity in EC‐containing concentroids, which better resemble the fetal human brain compared to classical organoids or NPC‐only concentroids. This PSC‐derived "vascularized" concentroid brain model will facilitate the study of neurovascular/blood‐brain barrier development, neural cell migration, and the development of effective in vitro vascularization strategies of brain mimics. [ABSTRACT FROM AUTHOR]

Background: In this observational study, we compared continuous physiological signals during an active standing test in adults aged 50 years and over, characterised as frail by three different criteria, using data from The Irish Longitudinal Study on Ageing (TILDA). Methods: This study utilised data from TILDA, an ongoing landmark prospective cohort study of community-dwelling adults aged 50 years or older in Ireland. The initial sampling strategy in TILDA was based on random geodirectory sampling. Four independent groups were identified: those characterised as frail only by one of the frailty tools used (the physical Frailty Phenotype (FP), the 32-item Frailty Index (FI), or the Clinical Frailty Scale (CFS) classification tree), and a fourth group where participants were not characterised as frail by any of these tools. Continuous non-invasive physiological signals were collected during an active standing test, including systolic (sBP) and diastolic (dBP) blood pressure, as well as heart rate (HR), using digital artery photoplethysmography. Additionally, the frontal lobe cerebral oxygenation (Oxy), deoxygenation (Deoxy), and tissue saturation index (TSI) were also non-invasively measured using near-infrared spectroscopy (NIRS). The signals were visualised across frailty groups and statistically compared using one-dimensional statistical parametric mapping (SPM). Results: A total of 1124 participants (mean age of 63.5 years; 50.2% women) were included: 23 were characterised as frail only by the FP, 97 by the FI, 38 by the CFS, and 966 by none of these criteria. The SPM analyses revealed that only the group characterised as frail by the FI had significantly different signals (p < 0.001) compared to the non-frail group. Specifically, they exhibited an attenuated gain in HR between 10 and 15 s post-stand and larger deficits in sBP and dBP between 15 and 20 s post-stand. Conclusions: The FI proved to be more adept at capturing distinct physiological responses to standing, likely due to its direct inclusion of cardiovascular morbidities in its definition. Significant differences were observed in the dynamics of cardiovascular signals among the frail populations identified by different frailty criteria, suggesting that caution should be taken when employing frailty identification tools on physiological signals, particularly the neurocardiovascular signals in an active standing test. [ABSTRACT FROM AUTHOR]

Introduction: Angiopoietin 1 (angpt1) is essential for angiogenesis. However, its role in neurogenesis is largely undiscovered. This study aimed to identify the role of angpt1 in brain development, the mode of action of angpt1, and its prime targets in the zebrafish brain. Methods: We investigated the effects of embryonic brain angiogenesis and neural development using qPCR, in situ hybridization, microangiography, retrograde labeling, and immunostaining in the angpt1sa14264, itgb1bmi371, tekhu1667 mutant fish and transgenic overexpression of angpt1 in the zebrafish larval brains. Results: We showed the co-localization of angpt1 with notch, delta, and nestin in the proliferation zone in the larval brain. Additionally, lack of angpt1 was associated with downregulation of TEK tyrosine kinase, endothelial (tek), and several neurogenic factors despite upregulation of integrin beta 1b (itgb1b), angpt2a, vascular endothelial growth factor aa (vegfaa), and glial markers. We further demonstrated that the targeted angpt1sa14264 and itgb1bmi371 mutant fish showed severely irregular cerebrovascular development, aberrant hindbrain patterning, expansion of the radial glial progenitors, downregulation of cell proliferation, deficiencies of dopaminergic, histaminergic, and GABAergic populations in the caudal hypothalamus. In contrast to angpt1sa14264 and itgb1bmi371 mutants, the tekhu1667 mutant fish regularly grew with no apparent phenotypes. Notably, the neural-specific angpt1 overexpression driven by the elavl3 (HuC) promoter significantly increased cell proliferation and neuronal progenitor cells but decreased GABAergic neurons, and this neurogenic activity was independent of its typical receptor tek. Discussion: Our results prove that angpt1 and itgb1b, besides regulating vascular development, act as a neurogenic factor via notch and wnt signaling pathways in the neural proliferation zone in the developing brain, indicating a novel role of dual regulation of angpt1 in embryonic neurogenesis that supports the concept of angiopoietin-based therapeutics in neurological disorders. [ABSTRACT FROM AUTHOR]

Purpose: Neurovascular MRI suffers from a rapid drop in B1+ into the neck when using transmit head coils at 7 T. One solution to improving B1+ magnitude in the major feeding arteries in the neck is to use custom RF shims on parallel‐transmit head coils. However, calculating such shims requires robust multichannel B1+ maps in both the head and the neck, which is challenging due to low RF penetration into the neck, limited dynamic range of multichannel B1+ mapping techniques, and B0 sensitivity. We therefore sought a robust, large‐dynamic‐range, parallel‐transmit field mapping protocol and tested whether RF shimming can improve carotid artery B1+ magnitude in practice. Methods: A pipeline is presented that combines B1+ mapping data acquired using circularly polarized (CP) and CP2‐mode RF shims at multiple voltages. The pipeline was evaluated by comparing the predicted and measured B1+ for multiple random transmit shims, and by assessing the ability of RF shimming to increase B1+ in the carotid arteries. Results: The proposed method achieved good agreement between predicted and measured B1+ in both the head and the neck. The B1+ magnitude in the carotid arteries can be increased by 43% using tailored RF shims or by 37% using universal RF shims, while also improving the RF homogeneity compared with CP mode. Conclusion: B1+ in the neck can be increased using RF shims calculated from multichannel B1+ maps in both the head and the neck. This can be achieved using universal phase‐only RF shims, facilitating easy implementation in existing sequences. [ABSTRACT FROM AUTHOR]

The hierarchical network of blood vessels comprises the larger vessels (veins and arteries), the smaller ones (venules and arterioles), and the thinnest capillaries. The proper functioning of most tissues in the body relies on vascularization, which is meant for the diffusion of gases, nutrients, and harmful waste. However, it is known that cell survival is compromised as the diffusion of oxygen is limited beyond 100–200 µm and damage can occur at any level of the complex system of the vascular network, as is the case in cardiovascular, musculoskeletal, and neurovascular diseases that recur and progress with age. These may prove fatal, hence the need for vascular tissue engineering (VTE) arises. VTE mainly focuses on the fabrication of vascular constructs using natural, synthetic material, or a combination of both using various techniques. The construct is expected to integrate and anastomose with the host vasculature. 4D bioprinting is an emerging field that allows the fabrication of hollow tubes employing different materials that respond to different stimuli. This review is a comprehensive summary of the major techniques employed in VTE and the recent technique of 4D bioprinting foreseen to revolutionize the field. [ABSTRACT FROM AUTHOR]

Aims: We sought to identify and optimise a universally available histological marker for pericytes in the human brain. Such a marker could be a useful tool for researchers. Further, identifying a gene expressed relatively specifically in human pericytes could provide new insights into the biological functions of this fascinating cell type. Methods: We analysed single‐cell RNA expression profiles derived from different human and mouse brain regions using a high‐throughput and low‐cost single‐cell transcriptome sequencing method called EasySci. Through this analysis, we were able to identify specific gene markers for pericytes, some of which had not been previously characterised. We then used commercially (and therefore universally) available antibodies to immunolabel the pericyte‐specific gene products in formalin‐fixed paraffin‐embedded (FFPE) human brains and also performed immunoblots to determine whether appropriately sized proteins were recognised. Results: In the EasySci data sets, highly pericyte‐enriched expression was notable for SLC6A12 and SLC19A1. Antibodies against these proteins recognised bands of approximately the correct size in immunoblots of human brain extracts. Following optimisation of the immunohistochemical technique, staining for both antibodies was strongly positive in small blood vessels and was far more effective than a PDGFRB antibody at staining pericyte‐like cells in FFPE human brain sections. In an exploratory sample of other human organs (kidney, lung, liver, muscle), immunohistochemistry did not show the same pericyte‐like pattern of staining. Conclusions: The SLC6A12 antibody was well suited for labelling pericytes in human FFPE brain sections, based on the combined results of single‐cell RNA‐seq analyses, immunoblots and immunohistochemical studies. [ABSTRACT FROM AUTHOR]

Migraine is a debilitating disorder that afflicts over 1 billion people worldwide, involving attacks that result in a throbbing and pulsating headache. Migraine is thought to be a neurovascular event associated with vasoconstriction, vasodilation, and neuronal activation. Understanding signaling in migraine pathology is central to the development of therapeutics for migraine prophylaxis and for mitigation of migraine in the prodrome phase before pain sets in. The fact that both vasoactivity and neural sensitization are involved in migraine indicates that agonists which promote these phenomena may very well be involved in migraine pathology. One such group of agonists is the purines, in particular, adenosine phosphates and their metabolites. This manuscript explores what is known about the relationship between these metabolites and migraine pathology and explores the potential for such relationships through their known signaling pathways. [ABSTRACT FROM AUTHOR]

IntroductionHolter-SRA (Stroke Risk Analysis) is an automated analysis of ECG monitoring for Atrial Fibrillation (AF) detection. The aim of this study was to evaluate the rate of AF in undetermined TIA/Rapidly improving stroke symptoms (RISS) patients.MethodsProspective study of undetermined TIA/RISS patients who presented to the emergency department. Early vascular studies (angio CT, transthoracic echocardiography and ECG) were performed in emergency department. The Holter-SRA device was placed for 2 h and the patients were classified into: confirmed AF, high risk of AF or low risk of AF. Prolonged ambulatory monitoring (7 days) was carried out every month for patients with a high-risk pattern. The results were evaluated until definitive detection of AF or low-risk pattern. The endpoints were rate of AF and vascular recurrence at 90 days.ResultsOver a period of 24 months, 83 undetermined TIA/RISS patients were enrolled. The mean age was 70 ± 10 years and 61% were men. The median ABCD2 score was 4 points (1–7). After 2 h of monitoring in the emergency department, AF was detected in one patient (1.2%), 51 patients with a low-risk pattern and 31 patients (37.3%) showed a high-risk pattern of AF. During the ambulatory monitoring, of the 31 patients high risk pattern patients, AF was diagnosed to 17 cases and of the 51 patients with a low-risk pattern, one case experienced a recurrent vascular due to undetected AF (1.9% false negative). Three patients (3.6%) suffered a vascular recurrence within the first 90 days, before AF diagnosis.ConclusionsIn our study, AF was detected in 22.9% of the 83 patients with indeterminate TIA/RISS. Holter-SRA has allowed us to increase the detection of AF, especially those patients with a high-risk pattern in the first 3 months.

Abstract Although human pluripotent stem cell (PSC)‐derived brain organoids have enabled researchers to gain insight into human brain development and disease, these organoids contain solely ectodermal cells and are not vascularized as occurs during brain development. Here it is created less complex and more homogenous large neural constructs starting from PSC‐derived neuroprogenitor cells (NPC), by fusing small NPC spheroids into so‐called concentroids. Such concentroids consisted of a pro‐angiogenic core, containing neuronal and outer radial glia cells, surrounded by an astroglia‐dense outer layer. Incorporating PSC‐derived endothelial cells (EC) around and/or in the concentroids promoted vascularization, accompanied by differential outgrowth and differentiation of neuronal and astroglia cells, as well as the development of ectodermal‐derived pericyte‐like mural cells co‐localizing with EC networks. Single nucleus transcriptomic analysis revealed an enhanced neural cell subtype maturation and diversity in EC‐containing concentroids, which better resemble the fetal human brain compared to classical organoids or NPC‐only concentroids. This PSC‐derived “vascularized” concentroid brain model will facilitate the study of neurovascular/blood‐brain barrier development, neural cell migration, and the development of effective in vitro vascularization strategies of brain mimics.

Neurovascular diseases are linked to the brain's blood vessels. These disorders are complicated to treat due to the strict selective characteristics of the blood–brain barrier. Consequently, the potency of the pharmacological treatments for these conditions is immensely diminished, leading to a rise in neurovascular-associated morbidity and mortality. Carbon nanotubes are regarded as essential nanoparticles with a promise of treating neurovascular disorders. Current findings have demonstrated the effectiveness of carbon nanotubes as vehicles for ferrying drugs to the site of interest. This review accentuates the theoretical utilisation of carbon nanotubes as drug nanocarriers equipped with the penetrating capability to the blood–brain barrier for treating neurovascular disorders such as ischemic stroke. The success of the carbon nanotube system may result in the development of a new and highly relevant drug delivery procedure. This review will also cover carbon nanotube functionalisation for applications in the biomedical fields, toxicity, in vitro and in vivo drugs and biomolecule delivery, and the future outlook of carbon nanotubes. [ABSTRACT FROM AUTHOR]

Although alcohol consumption during pregnancy is a major cause of behavioral and learning disabilities, most FASD infants are late- or even misdiagnosed due to clinician's difficulties achieving early detection of alcohol-induced neurodevelopmental impairments. Neuroplacentology has emerged as a new field of research focusing on the role of the placenta in fetal brain development. Several studies have reported that prenatal alcohol exposure (PAE) dysregulates a functional placenta–cortex axis, which is involved in the control of angiogenesis and leads to neurovascular-related defects. However, these studies were focused on PlGF, a pro-angiogenic factor. The aim of the present study is to provide the first transcriptomic "placenta–cortex" signature of the effects of PAE on fetal angiogenesis. Whole mouse genome microarrays of paired placentas and cortices were performed to establish the transcriptomic inter-organ "placenta–cortex" signature in control and PAE groups at gestational day 20. Genespring comparison of the control and PAE signatures revealed that 895 and 1501 genes were only detected in one of two placenta–cortex expression profiles, respectively. Gene ontology analysis indicated that 107 of these genes were associated with vascular development, and String protein–protein interaction analysis showed that they were associated with three functional clusters. PANTHER functional classification analysis indicated that "intercellular communication" was a significantly enriched biological process, and 27 genes were encoded for neuroactive ligand/receptors interactors. Protein validation experiments involving Western blot for one ligand–receptor couple (Agt/AGTR1/2) confirmed the transcriptomic data, and Pearson statistical analysis of paired placentas and fetal cortices revealed a negative correlation between placental Atg and cortical AGTR1, which was significantly impacted by PAE. In humans, a comparison of a 38WG control placenta with a 36WG alcohol-exposed placenta revealed low Agt immunolabeling in the syncytiotrophoblast layer of the alcohol case. In conclusion, this study establishes the first transcriptomic placenta–cortex signature of a developing mouse. The data show that PAE markedly unbalances this inter-organ signature; in particular, several ligands and/or receptors involved in the control of angiogenesis. These data support that PAE modifies the existing communication between the two organs and opens new research avenues regarding the impact of placental dysfunction on the neurovascular development of fetuses. Such a signature would present a clinical value for early diagnosis of brain defects in FASD. [ABSTRACT FROM AUTHOR]

A 6-year-old neutered male German shepherd dog was evaluated for obtundation, blindness, and bilateral exophthalmos. A magnetic resonance imaging scan of the brain was performed and identified an arteriovenous malformation (AVM) with several feeding arterial branches, and venous drainage through the cavernous sinus. Venous vessels rostral to the AVM were severely distended and extended into the retrobulbar spaces. Liquid embolization by injection of ethylene vinyl alcohol copolymer was performed from access points in the maxillary arteries and internal carotid arteries. No intraprocedural complications were encountered, and the dog was discharged the next day. Bilateral enucleation eventually was performed because of exposure keratopathy. At 31 months post-embolization, owners reported that the dog was doing very well clinically with high activity level and normal appetite, and the dog also appeared to be pain free. Although intracranial AVMs are very rare in companion animals, successful treatment using liquid embolization is possible and should be considered.

Onboard oxygen-generating systems (OBOGSs) provide increased inspired oxygen (FiO2) to mitigate the risk of neurologic injury in high altitude aviators. OBOGSs can deliver highly variable oxygen concentrations oscillating around a predetermined FiO2 set point, even when the aircraft cabin altitude is relatively stable. Steady-state exposure to 100% FiO2 evokes neurovascular vasoconstriction, diminished cerebral perfusion, and altered electroencephalographic activity. Whether non-steady-state FiO2 exposure leads to similar outcomes is unknown. This study characterized the physiologic responses to steady-state and non-steady-state FiO2 during normobaric and hypobaric environmental pressures emulating cockpit pressures within tactical aircraft. The participants received an indwelling radial arterial catheter while exposed to steady-state or non-steady-state FiO2 levels oscillating ± 15% of prescribed set points in a hypobaric chamber. Steady-state exposure to 21% FiO2 during normobaria produced arterial blood gas values within the anticipated ranges. Exposure to non-steady-state FiO2 led to PaO2 levels higher upon cessation of non-steady-state FiO2 than when measured during steady-state exposure. This pattern was consistent across all FiO2 ranges, at each barometric condition. Prefrontal cortical activation during cognitive testing was lower following exposure to non-steady-state FiO2 >50% and iO2 levels >50% reduced prefrontal cortical brain activation during the cognitive challenge, consistent with an evoked pattern of neurovascular constriction and dilation.

Intercellular influences are necessary for coordinated development and function of vascular and neural components in the brain. In the early postnatal period after birth, the mammalian cerebellum undergoes extensive morphogenesis — developing its characteristic lobules, organizing its diverse cell types into defined cellular layers, and establishing neural circuits that support cerebellar function, such as coordinated movement. In parallel, the cerebellar vasculature undergoes extensive postnatal growth and maturation, keeping pace with the expanding neural compartment. Endothelial deletion of Rbpj leads to neurovascular abnormalities in mice, including arteriovenous (AV) shunts that supplant capillaries and instead direct high-pressure/high-flow arterial blood directly to veins. Gross and histopathological cerebellar abnormalities, associated with these Rbpj-mediated brain AV malformations (AVMs), led to our hypothesis that early postnatal morphogenesis and lamination of cerebellum was perturbed in mice harboring endothelial Rbpj deficiency from birth. Here, we show that endothelial Rbpj-mutant mice developed enlarged vascular malformations on the cerebellar surface, by 2-week post-Rbpj deletion. In addition, outgrowth of cerebellar lobules was impaired through decreased cell proliferation, but not increased apoptosis, in the external granule layer. Molecular layer thickness was reduced, and the Purkinje layer was affected, by decreased Purkinje cell number, primary dendrite length, and dendritic arbor density. Endothelial deletion of Rbpj also led to impaired motor behaviors, consistent with abnormal cerebellar morphogenesis and lamination. Thus, our data suggest that Rbpj is required, in early postnatal vascular endothelium, to ensure proper cerebellar outgrowth, morphogenesis, and function in mice. [ABSTRACT FROM AUTHOR]

Ischemic stroke is among the common comorbidities of HIV-1 infection. People with HIV (PWH) experience increased stroke susceptibility, more severe ischemic stroke outcomes, and delayed recovery after a stroke. The gut microbiota and the central nervous system exhibit a bidirectional relationship, which is affected by both HIV-1 and ischemic stroke. The NLRP3 inflammasome is a key mediator in the microbiota–gut–brain axis. HIV-1 infection can lead to gut dysbiosis and activation of the NLRP3 inflammasome, making PWH more susceptible to comorbidities and infections due to the integral involvement of the gastrointestinal tract in the body's immune system. Alterations in the gut microbiota may contribute to the severity of a stroke. It is hypothesized that the efficacy of ischemic stroke treatment may be improved when coupled with maintenance of the gut's homeostasis. Blocking the NLRP3 inflammasome serves as a potential treatment for preventing neurological decline after a stroke. HIV-associated comorbidities, such as ischemic stroke, are prevalent in people with HIV (PWH). Several studies both in animal models and humans have revealed an association between activation of the inflammasome in HIV-1 infection and stroke. The gut microbiota is an important component in controlling neuroinflammation in the CNS. It has also been proposed to be involved in the pathobiology of HIV-1 infection, and has been associated with an increase in activation of the inflammasome. In this review, we provide an overview of the microbiota–gut–inflammasome–brain axis, focusing on the NLRP3 inflammasome and dysregulation of the microbiome as risk factors that may contribute to the outcome of ischemic stroke and recovery in PWH. We also focus on the potential of targeting the NLRP3 inflammasome as a novel therapeutic approach for PWH who are at risk of developing cerebrovascular diseases. [ABSTRACT FROM AUTHOR]

• Cerebral revascularization remains an important tool in the neurosurgical armamentarium. • Selecting the optimal donor, recipient, and approach are vital to successful anastomosis. • The STA, MMA, and OA can be used to augment or replace cranial circulation. • A mathematical model can be used to analyze and grade donor-recipient vessel pairs. • A flow-based algorithm for donor selection can help determine donor suitability. Utilization an in-situ pedicle of the external carotid artery (ECA) as an arterial donor can allow for the successful augmentation or replacement of flow to a large vascular territory. We propose a mathematical model for quantitatively analyzing and grading the suitability of donor and recipient bypass vessels based on a set of anatomical and surgical variables in order to predict which pair has the greatest possibility for success. Using this method, we analyze all of the potential donor-recipient pairs for each ECA donor vessel—including the superficial temporal (STA), middle meningeal (MMA), and occipital (OA) arteries. The ECA pedicles were dissected in frontotemporal, middle fossa, subtemporal, retrosigmoid, far lateral, suboccipital, supracerebellar, and occipital transtentorial approaches. For each approach, every potential donor-recipient pair was identified, and donor length and diameter were measured as well as depth of field, angle of exposure, ease of proximal control, maneuverability, and length and diameter of the recipient segment. Anastomotic pair scores were determined by adding the weighted donor and recipient. The best overall anastomotic pairs were OA-vertebral artery (V3, 17.1) and STA-insular (M2, 16.3) and STA-sylvian (M3, 15.9) segments of the middle cerebral artery. Other strong anastomotic combinations were OA- telovelotonsillar (15) and OA- tonsilomedullary (14.9) segments of the posterior inferior cerebellar artery, and MMA-lateral pontomesencephalic segment of the superior cerebellar artery (14.2). This novel model for anastamotic pair scoring can serve as a useful clinical tool for selecting the optimal donor, recipient, and approach combination that can help facilitate a successful bypass. [ABSTRACT FROM AUTHOR]

Purpose: Retinal vein occlusion (RVO) is a sight-threatening condition typically treated with intravitreal injection of vascular endothelial growth factor (VEGF) antagonists. Treatment response to anti-VEGF therapies is highly variable, with poor visual outcomes and treatment response in patients with significant retinal nonperfusion following RVO. Recently, caspase-9 has been identified as a potent regulator of edema, gliosis, and neuronal dysfunction during acute retinal hypoxia. The purpose of this study was to compare the therapeutic effect of caspase-9 inhibition against VEGF-neutralization in an established mouse model of RVO. Methods: Adult male C57Bl/6 J mice were randomized to induction of RVO and treatment with either vehicle, intravitreal injection of anti-VEGF antibody, topical administration of a selective caspase-9 inhibitor (Pen1-XBir3), or a combination therapy. Animals were followed on days 1, 2, and 8 after RVO with fundus retinal imaging, and with optical coherence tomography (OCT) to capture retinal swelling, capillary nonperfusion (measured by disorganization of retinal inner layers, DRIL), hyperreflective foci (HRF), and retinal atrophy. Focal electroretinography (ERG) measurements were performed on day 7. Histology was performed on retinal sections from day 8. Results: Both VEGF neutralization and caspase-9 inhibition showed significant retinal protection from RVO compared to vehicle treatment arm. Retinal reperfusion of occluded veins was accelerated in eyes receiving caspase-9 inhibitor, but not significantly different from vehicle in the anti-VEGF group. Retinal edema was suppressed in all treatment groups, with approximately 2-fold greater edema reduction with caspase-9 inhibition compared to VEGF neutralization. HRF were reduced similarly across all treatment groups compared to vehicle. Retinal detachment was reduced only in eyes treated with caspase-9 inhibitor monotherapy. Caspase-9 inhibition reduced retinal atrophy and preserved ERG response; VEGF neutralization did not prevent neurodegeneration following RVO. Conclusion: Caspase-9 inhibition confers stronger neuronal and vascular protection compared to VEGF neutralization in the mouse laser-induced model of RVO. [ABSTRACT FROM AUTHOR]

Background: Surgical mortality indicators should be risk-adjusted when evaluating the performance of organisations. This study evaluated the performance of risk-adjustment models that used English hospital administrative data for 30-day mortality after neurosurgery. Methods: This retrospective cohort study used Hospital Episode Statistics (HES) data from 1 April 2013 to 31 March 2018. Organisational-level 30-day mortality was calculated for selected subspecialties (neuro-oncology, neurovascular and trauma neurosurgery) and the overall cohort. Risk adjustment models were developed using multivariable logistic regression and incorporated various patient variables: age, sex, admission method, social deprivation, comorbidity and frailty indices. Performance was assessed in terms of discrimination and calibration. Results: The cohort included 49,044 patients. Overall, 30-day mortality rate was 4.9%, with unadjusted organisational rates ranging from 3.2 to 9.3%. The variables in the best performing models varied for the subspecialties; for trauma neurosurgery, a model that included deprivation and frailty had the best calibration, while for neuro-oncology a model with these variables plus comorbidity performed best. For neurovascular surgery, a simple model of age, sex and admission method performed best. Levels of discrimination varied for the subspecialties (range: 0.583 for trauma and 0.740 for neurovascular). The models were generally well calibrated. Application of the models to the organisation figures produced an average (median) absolute change in mortality of 0.33% (interquartile range (IQR) 0.15–0.72) for the overall cohort model. Median changes for the subspecialty models were 0.29% (neuro-oncology, IQR 0.15–0.42), 0.40% (neurovascular, IQR 0.24–0.78) and 0.49% (trauma neurosurgery, IQR 0.23–1.68). Conclusions: Reasonable risk-adjustment models for 30-day mortality after neurosurgery procedures were possible using variables from HES, although the models for trauma neurosurgery performed less well. Including a measure of frailty often improved model performance. [ABSTRACT FROM AUTHOR]

Ultrasound imaging is a critical tool for triaging and diagnosing subjects but only if images can be properly interpreted. Unfortunately, in remote or military medicine situations, the expertise to interpret images can be lacking. Machine-learning image interpretation models that are explainable to the end user and deployable in real time with ultrasound equipment have the potential to solve this problem. We have previously shown how a YOLOv3 (You Only Look Once) object detection algorithm can be used for tracking shrapnel, artery, vein, and nerve fiber bundle features in a tissue phantom. However, real-time implementation of an object detection model requires optimizing model inference time. Here, we compare the performance of five different object detection deep-learning models with varying architectures and trainable parameters to determine which model is most suitable for this shrapnel-tracking ultrasound image application. We used a dataset of more than 16,000 ultrasound images from gelatin tissue phantoms containing artery, vein, nerve fiber, and shrapnel features for training and evaluating each model. Every object detection model surpassed 0.85 mean average precision except for the detection transformer model. Overall, the YOLOv7tiny model had the higher mean average precision and quickest inference time, making it the obvious model choice for this ultrasound imaging application. Other object detection models were overfitting the data as was determined by lower testing performance compared with higher training performance. In summary, the YOLOv7tiny object detection model had the best mean average precision and inference time and was selected as optimal for this application. Next steps will implement this object detection algorithm for real-time applications, an important next step in translating AI models for emergency and military medicine. [ABSTRACT FROM AUTHOR]

Objectives The canalis sinuosus (CS) is an auxiliary canal that encompasses the anterior superior alveolar nerve, artery, and vein. Understanding the location of this neurovascular structure during surgery can help prevent severe complications. This study aimed to assess the frequency, location, and classification of the CS using CBCT images. Methods CBCT images of 200 patients were examined considering factors, such as age, sex, presence of impacted teeth, the diameter of the canal’s orifice, and the location of the CS. In sagittal images, the distance from the CS to the buccal cortex, nasal floor, and alveolar crest was measured. Statistical analyses were conducted to compare variables between males and females, as well as between the right and left sides. The Chi-square, Fisher’s exact test, Wilcoxon test, paired t-test, and Kruskal-Wallis tests were utilized for data analysis at a significance level of 5%. Results The CS was detected in 135 cases (67.5%) on both sides, while it was not visible in 19 cases (9.5%). In 46 images (23%), the CS was observed only on one side. The canal was most commonly located in the lateral incisor region, followed by the canine area. The average distance from the canal’s orifice to anatomical landmarks, such as the alveolar crest, buccal cortex, and nasal floor, was greater in males than in females. However, this difference was not significant between the right and left sides (P=0.56, P=0.31, P=0.98; respectively). When comparing males and females, no significant differences were observed in the occurrence of CS(P=0.728), the diameter of the canal(P=0.114), the buccopalatal position of the CS(P=0.800), or the canal location within the arch(P=0.132). Conclusion It appears that CBCT and other 3D imaging techniques are essential for detecting the CS prior to performing surgery in the anterior maxillary region. [ABSTRACT FROM AUTHOR]

Intracranial venous pathologies are a historically underrecognized group of disorders that can have a devastating impact on patients. Despite advancements in peripheral venous disorders and arterial neurointerventions, intracranial venous pathologies have received comparatively little attention. Understanding the anatomy, physiology, clinical relevance, and treatment options of intracranial venous pathologies is fundamental to evolving therapies and research priorities. This article provides an overview of major intracranial venous pathologies, the respective pathophysiologies, and treatment options. [ABSTRACT FROM AUTHOR]

Photon-counting detector (PCD) is a novel computed tomography detector technology (photon-counting computed tomography—PCCT) that presents many advantages in the neurovascular field, such as increased spatial resolution, reduced radiation exposure, and optimization of the use of contrast agents and material decomposition. In this overview of the existing literature on PCCT, we describe the physical principles, the advantages and the disadvantages of conventional energy integrating detectors and PCDs, and finally, we discuss the applications of the PCD, focusing specifically on its implementation in the neurovascular field. [ABSTRACT FROM AUTHOR]

Advanced visualization techniques such as maximum intensity projection (MIP) and volume rendering (VR) are useful for evaluating neurovascular anatomy on CT angiography (CTA) of the brain; however, interference from surrounding osseous anatomy is common. Existing methods for removing bone from CTA images are limited in scope and/or accuracy, particularly at the skull base. We present a new brain CTA bone removal tool, which addresses many of these limitations. A deep convolutional neural network was designed and trained for bone removal using 72 brain CTAs. The model was tested on 15 CTAs from the same data source and 17 CTAs from an independent external dataset. Bone removal accuracy was assessed quantitatively, by comparing automated segmentation results to manual segmentations, and qualitatively by evaluating VR visualization of the carotid siphons compared to an existing method for automated bone removal. Average Dice overlap between automated and manual segmentations from the internal and external test datasets were 0.986 and 0.979 respectively. This was superior compared to a publicly available noncontrast head CT bone removal algorithm which had a Dice overlap of 0.947 (internal dataset) and 0.938 (external dataset). Our algorithm yielded better VR visualization of the carotid siphons than the publicly available bone removal tool in 14 out of 15 CTAs (93%, chi-square statistic of 22.5, p-value of < 0.00001) from the internal test dataset and 15 out of 17 CTAs (88%, chi-square statistic of 23.1, p-value of < 0.00001) from the external test dataset. Bone removal allowed subjectively superior MIP and VR visualization of vascular anatomy/pathology. The proposed brain CTA bone removal algorithm is rapid, accurate, and allows superior visualization of vascular anatomy and pathology compared to other available techniques and was validated on an independent external dataset. [ABSTRACT FROM AUTHOR]

Objective: Acute renal in-stent thrombosis is common, especially after complex endovascular treatments, or in case of risk factors such as Covid-19 infection. Irreversible renal damage occurred when the renal artery was occluded for more than 3 hours. In this case, we present a case of renal function recovery after thromboaspiration of a renal stent thrombosis for more than 72 hours. Case presentation: A 88-year-old man who tested positive for COVID-19 presented to the emergency room with dyspnea and anuria. He referred a previous complex endovascular intervention with the triple chimney technique (ChEVAR). More than 72 hours passed between the onset of symptoms to the diagnosis of acute renal intra-stent thrombosis. He underwent urgent thromboaspiration with neurovascular devices returning to his baseline renal function. Conclusion: Despite the prolonged ischemia, renal revascularization with thromboaspiration restored renal function and rescued the remaining renal parenchyma. [ABSTRACT FROM AUTHOR]

This third in a series of vascular cognitive impairment (VCI) workshops, supported by "The Leo and Anne Albert Charitable Trust," was held from February 8 to 12 at the Omni Resort in Carlsbad, CA. This workshop followed the information gathered from the earlier two workshops suggesting that we focus more specifically on brain white matter in age-related cognitive impairment. The Scientific Program Committee (Frank Barone, Shawn Whitehead, Eric Smith, and Rod Corriveau) assembled translational, clinical, and basic scientists with unique expertise in acute and chronic white matter injury at the intersection of cerebrovascular and neurodegenerative etiologies. As in previous Albert Trust workshops, invited participants addressed key topics related to mechanisms of white matter injury, biomarkers of white matter injury, and interventions to prevent white matter injury and age-related cognitive decline. This report provides a synopsis of the presentations and discussions by the participants, including the existing knowledge gaps and the delineation of the next steps towards advancing our understanding of white matter injury and age-related cognitive decline. Workshop discussions and consensus resulted in action by The Albert Trust to (1) increase support from biannual to annual "White Matter and Cognition" workshops; (2) provide funding for two collaborative, novel research grants annually submitted by meeting participants; and (3) coordinate the formation of the "Albert Research Institute for White Matter and Cognition." This institute will fill a gap in white matter science, providing white matter and cognition communications, including annual updates from workshops and the literature and interconnecting with other Albert Trust scientific endeavors in cognition and dementia, and providing support for newly established collaborations between seasoned investigators and to the development of talented young investigators in the VCI-dementia (VCID) and white matter cognition arena.