Germinal Matrix Hemorrhage Research Articles

Retrospective evaluation of newborns with germinal matrix hemorrhage after preterm delivery

Amaç: Bu çalışmada germinal matriks kanaması olan hastaların klinik seyri ve tedavi sonuçlarını değerlendirmek amaçlanmıştır. Gereç ve Yöntem: Ocak 2018 – Mart 2020 tarihleri arasında germinal matriks kanaması olan hastalar retrospektif olarak incelenmiştir. Bulgular: Toplam 66 hasta germinal matriks kanaması nedeni ile takip edildi. Hastaların 34’ü kadın, 32’si erkekti. On sekiz hastanın evre-1, 22 hastanın evre-2, 16 hastanın evre-3 ve 10 hastanın evre-4 kanaması vardı. Yirmi altı hastaya ventriküler tap yapıldı. On üç hastaya eksternal ventriküler drenaj takıldı. Bir hastaya ventriküler rezervuar ve bir hastaya ventrikülosubgaleal şant takıldı. Takiplerinde sekiz hastaya ventriküloperitoneal şant takıldı. Otuz altı hasta exitus oldu. Yirmi beş hasta taburcu edildi. Beş hasta dış merkeze sevk edildi. Sonuç: Preterm doğum sonrası germinal matriks kanamaları sık görülmekte ve asemptomatik olabilmektedir. Hastaların transfontanel ultrasonografi ile değerlendirilmeleri erken tanı ve tedavi olanağı sağlamaktadır. Bu hastaların tedavileri konusunda ortak bir algoritma henüz bulunmamaktadır.

A Case of Rapidly Resolving Abnormal Vertical Eye Movements in a Late-Preterm Neonate with Germinal Matrix Hemorrhages.

A Case of Rapidly Resolving Abnormal Vertical Eye Movements in a Late-Preterm Neonate with Germinal Matrix Hemorrhages.

GW0742 reduces mast cells degranulation and attenuates neurological impairments via PPARβ/δ/CD300a/SHP1 pathway after GMH in neonatal rats

BackgroundActivation of mast cells plays an important role in brain inflammation. CD300a, an inhibitory receptor located on mast cell surfaces, has been reported to reduce the production of pro-inflammatory cytokines and exert protective effects in inflammation-related diseases. Peroxisome proliferator–activated receptor β/δ (PPARβ/δ), a ligand-activated nuclear receptor, activation upregulates the transcription of CD300a. In this study, we aim to investigate the role of PPARβ/δ in the attenuation of germinal matrix hemorrhage (GMH)-induced mast cell activation via CD300a/SHP1 pathway. MethodsGMH model was induced by intraparenchymal injection of bacterial collagenase into the right hemispheric ganglionic eminence in P7 Sprague Dawley rats. GW0742, a PPARβ/δ agonist, was administered intranasally at 1 h post-ictus. CD300a small interfering RNA (siRNA) and PPARβ/δ siRNA were injected intracerebroventricularly 5 days and 2 days before GMH induction. Behavioral tests, Western blot, immunofluorescence, Toluidine Blue staining, and Nissl staining were applied to assess post-GMH evaluation. ResultsResults demonstrated that endogenous protein levels of PPARβ/δ and CD300a were decreased, whereas chymase, tryptase, IL-17A and transforming growth factor β1 (TGF-β1) were elevated after GMH. GMH induced significant short- and long-term neurobehavioral deficits in rat pups. GW0742 decreased mast cell degranulation, improved neurological outcomes, and attenuated ventriculomegaly after GMH. Additionally, GW0742 increased expression of PPARβ/δ, CD300a and phosphorylation of SHP1, decreased phosphorylation of Syk, chymase, tryptase, IL-17A and TGF-β1 levels. PPARβ/δ siRNA and CD300a siRNA abolished the beneficial effects of GW0742. ConclusionsGW0742 inhibited mast cell-induced inflammation and improved neurobehavior after GMH, which is mediated by PPARβ/δ/CD300a/SHP1 pathway. GW0742 may serve as a potential treatment to reduce brain injury for GMH patients.

Recombinant Slit2 suppresses neuroinflammation and Cdc42-mediated brain infiltration of peripheral immune cells via Robo1–srGAP1 pathway in a rat model of germinal matrix hemorrhage

BackgroundGerminal matrix hemorrhage (GMH) is a devastating neonatal stroke, in which neuroinflammation is a critical pathological contributor. Slit2, a secreted extracellular matrix protein, plays a repulsive role in axon guidance and leukocyte chemotaxis via the roundabout1 (Robo1) receptor. This study aimed to explore effects of recombinant Slit2 on neuroinflammation and the underlying mechanism in a rat model of GMH.MethodsGMH was induced by stereotactically infusing 0.3 U of bacterial collagenase into the germinal matrix of 7-day-old Sprague Dawley rats. Recombinant Slit2 or its vehicle was administered intranasally at 1 h after GMH and daily for 3 consecutive days. A decoy receptor recombinant Robo1 was co-administered with recombinant Slit2 after GMH. Slit2 siRNA, srGAP1 siRNA or the scrambled sequences were administered intracerebroventricularly 24 h before GMH. Neurobehavior, brain water content, Western blotting, immunofluorescence staining and Cdc42 activity assays were performed.ResultsThe endogenous brain Slit2 and Robo1 expressions were increased after GMH. Robo1 was expressed on neuron, astrocytes and infiltrated peripheral immune cells in the brain. Endogenous Slit2 knockdown by Slit2 siRNA exacerbated brain edema and neurological deficits following GMH. Recombinant Slit2 (rSlit2) reduced neurological deficits, proinflammatory cytokines, intercellular adhesion molecules, peripheral immune cell markers, neuronal apoptosis and Cdc42 activity in the brain tissue after GMH. The anti-neuroinflammation effects were reversed by recombinant Robo1 co-administration or srGAP1 siRNA.ConclusionsRecombinant Slit2 reduced neuroinflammation and neuron apoptosis after GMH. Its anti-neuroinflammation effects by suppressing onCdc42-mediated brain peripheral immune cells infiltration was at least in part via Robo1–srGAP1 pathway. These results imply that recombinant Slit2 may have potentials as a therapeutic option for neonatal brain injuries.

The impact of red blood cell transfusion in preterm neonates on germinal matrix hemorrhage: incidence and grade with correlation to outcome

BackgroundGerminal matrix hemorrhage affects 20 to 25% of infants with a low birth weight (less than 1500 g). About one-tenth of them progress to intra-parenchymal hemorrhage, usually during the first days after birth. Several studies have found a correlation between packed RBC transfusions and a higher frequency of severe germinal matrix hemorrhage in neonatal intensive care units.Transcranial ultrasound is a safe, noninvasive modality that can be used repeatedly in the neonates with ability to detect different grades of germinal matrix hemorrhage.ObjectiveWas to evaluate the impact of packed RBC transfusion on the incidence and grade of germinal matrix hemorrhage, as evaluated by transcranial Doppler, and correlation to outcome.MethodsThis prospective observational study included one hundred preterm infants admitted to NICU, suffering from GM hemorrhage throughout 9 months duration. Bedside transcranial ultrasound was done for all the patients with a correlation of the grade of hemorrhage to the onset of blood transfusion, different clinical parameters, and the outcome.ResultsStatistical analysis showed a significant relation between the age of the first PRBC transfusion and GM hemorrhage grade. A positive relation was found between total amounts of PRBC transfusion and increasing grade of GM hemorrhage. A negative relation was found between GM hge grades and Apgar scores. GM hge patients who received PRBC transfusion had lower mean birth weight, lower gestational age, and longer duration of hospital stay than those who have not received PRBC transfusion.ConclusionClose monitoring of preterm neonates receiving packed RBCs, by transcranial ultrasound, as early as possible, is mandatory to early detect GM hge and limit subsequent morbidities.

124 A Role for P-selectin and complement in the pathological sequelae of Germinal Matrix Hemorrhage

124 A Role for P-selectin and complement in the pathological sequelae of Germinal Matrix Hemorrhage

127 Complement drives chronic inflammation and progressive hydrocephalus in murine neonatal germinal matrix hemorrhage

127 Complement drives chronic inflammation and progressive hydrocephalus in murine neonatal germinal matrix hemorrhage

Pharmacological pain and sedation interventions for the prevention of intraventricular hemorrhage in preterm infants on assisted ventilation - an overview of systematic reviews.

Pharmacological pain and sedation interventions for the prevention of intraventricular hemorrhage in preterm infants on assisted ventilation - an overview of systematic reviews.

Fractalkine Enhances Hematoma Resolution and Improves Neurological Function via CX3CR1/AMPK/PPARγ Pathway After GMH.

Hematoma clearance has been a proposed therapeutic strategy for hemorrhagic stroke. This study investigated the impact of CX3CR1 (CX3C chemokine receptor 1) activation mediated by r-FKN (recombinant fractalkine) on hematoma resolution, neuroinflammation, and the underlying mechanisms involving AMPK (AMP-activated protein kinase)/PPARγ (peroxisome proliferator-activated receptor gamma) pathway after experimental germinal matrix hemorrhage (GMH). A total of 313 postnatal day 7 Sprague Dawley rat pups were used. GMH was induced using bacterial collagenase by a stereotactically guided infusion. r-FKN was administered intranasally at 1, 25, and 49 hours after GMH for short-term neurological evaluation. Long-term neurobehavioral tests (water maze, rotarod, and foot-fault test) were performed 24 to 28 days after GMH with the treatment of r-FKN once daily for 7 days. To elucidate the underlying mechanism, CX3CR1 CRISPR, or selective CX3CR1 inhibitor AZD8797, was administered intracerebroventricularly 24 hours preinduction of GMH. Selective inhibition of AMPK/PPARγ signaling in microglia via intracerebroventricularly delivery of liposome-encapsulated specific AMPK (Lipo-Dorsomorphin), PPARγ (Lipo-GW9662) inhibitor. Western blot, Immunofluorescence staining, Nissl staining, Hemoglobin assay, and ELISA assay were performed. The brain expression of FKN and CX3CR1 were elevated after GMH. FKN was expressed on both neurons and microglia, whereas CX3CR1 was mainly expressed on microglia after GMH. Intranasal administration of r-FKN improved the short- and long-term neurobehavioral deficits and promoted M2 microglia polarization, thereby attenuating neuroinflammation and enhancing hematoma clearance, which was accompanied by an increased ratio of p-AMPK (phosphorylation of AMPK)/AMPK, Nrf2 (nuclear factor erythroid 2-related factor 2), PPARγ, CD36 (cluster of differentiation 36), CD163 (hemoglobin scavenger receptor), CD206 (the mannose receptor), and IL (interleukin)-10 expression, and decreased CD68 (cluster of differentiation 68), IL-1β, and TNF (tumor necrosis factor) α expression. The administration of CX3CR1 CRISPR or CX3CR1 inhibitor (AZD8797) abolished the protective effect of FKN. Furthermore, selective inhibition of microglial AMPK/PPARγ signaling abrogated the anti-inflammation effects of r-FKN after GMH. CX3CR1 activation by r-FKN promoted hematoma resolution, attenuated neuroinflammation, and neurological deficits partially through the AMPK/PPARγ signaling pathway, which promoted M1/M2 microglial polarization. Activating CX3CR1 by r-FKN may provide a promising therapeutic approach for treating patients with GMH.

Role of N-formyl peptide receptor 2 in germinal matrix hemorrhage: an intrinsic review of a hematoma resolving pathway.

Germinal matrix hemorrhage is one of the leading causes of morbidity, mortality, and acquired infantile hydrocephalus in preterm infants in the United States, with little progress made in its clinical management. Blood clots have been shown to elicit secondary brain injury after germinal matrix hemorrhage, by disrupting normal cerebrospinal fluid circulation and absorption after germinal matrix hemorrhage causing post-hemorrhagic hydrocephalus development. Current evidence suggests that rapid hematoma resolution is necessary to improve neurological outcomes after hemorrhagic stroke. Various articles have demonstrated the beneficial effects of stimulating the polarization of microglia cells into the M2 phenotype, as it has been suggested that they play an essential role in the rapid phagocytosis of the blood clot after hemorrhagic models of stroke. N-formyl peptide receptor 2 (FPR2), a G-protein-coupled receptor, has been shown to be neuroprotective after stroke. FPR2 activation has been associated with the upregulation of phagocytic macrophage clearance, yet its mechanism has not been fully explored. Recent literature suggests that FPR2 may play a role in the stimulation of scavenger receptor CD36. Scavenger receptor CD36 plays a vital role in microglia phagocytic blood clot clearance after germinal matrix hemorrhage. FPR2 has been shown to phosphorylate extracellular-signal-regulated kinase 1/2 (ERK1/2), which then promotes the transcription of the dual-specificity protein phosphatase 1 (DUSP1) gene. In this review, we present an intrinsic outline of the main components involved in FPR2 stimulation and hematoma resolution after germinal matrix hemorrhage.

A role for P-selectin and complement in the pathological sequelae of germinal matrix hemorrhage

BackgroundGerminal matrix hemorrhage is a devastating disease of pre-term infancy commonly resulting in post-hemorrhagic hydrocephalus, periventricular leukomalacia, and subsequent neurocognitive deficits. We demonstrate vascular expression of the adhesion molecule P-selectin after GMH and investigate a strategy to specifically target complement inhibition to sites of P-selectin expression to mitigate the pathological sequelae of GMH.MethodsWe prepared two fusion proteins consisting of different anti-P-selectin single chain antibodies (scFv’s) linked to the complement inhibitor Crry. One scFv targeting vehicle (2.12scFv) blocked the binding of P-selectin to its PSGL-1 ligand expressed on leukocytes, whereas the other targeting vehicle (2.3scFv) bound P-selectin without blocking ligand binding. Post-natal C57BL/6 J mice on day 4 (P4) were subjected to collagenase induced-intraventricular hemorrhage and treated with 2.3Psel-Crry, 2.12Psel-Crry, or vehicle.ResultsCompared to vehicle treatment, 2.3Psel-Crry treatment after induction of GMH resulted in reduced lesion size and mortality, reduced hydrocephalus development, and improved neurological deficit measurements in adolescence. In contrast, 2.12Psel-Crry treatment resulted in worse outcomes compared to vehicle. Improved outcomes with 2.3Psel-Crry were accompanied by decreased P-selectin expression, and decreased complement activation and microgliosis. Microglia from 2.3Psel-Crry treated mice displayed a ramified morphology, similar to naïve mice, whereas microglia in vehicle treated animals displayed a more ameboid morphology that is associated with a more activated status. Consistent with these morphological characteristics, there was increased microglial internalization of complement deposits in vehicle compared to 2.3Psel-Crry treated animals, reminiscent of aberrant C3-dependent microglial phagocytosis that occurs in other (adult) types of brain injury. In addition, following systemic injection, 2.3Psel-Crry specifically targeted to the post-GMH brain. Likely accounting for the unexpected finding that 2.12Psel-Crry worsens outcome following GMH was the finding that this construct interfered with coagulation in this hemorrhagic condition, and specifically with heterotypic platelet–leukocyte aggregation, which express P-selectin and PSGL-1, respectively.ConclusionsGMH induces expression of P-selectin, the targeting of which with a complement inhibitor protects against pathogenic sequelae of GMH. A dual functioning construct with both P-selectin and complement blocking activity interferes with coagulation and worsens outcomes following GMH, but has potential for treatment of conditions that incorporate pathological thrombotic events, such as ischemic stroke.

Complement Drives Chronic Inflammation and Progressive Hydrocephalus in Murine Neonatal Germinal Matrix Hemorrhage.

Germinal matrix hemorrhage (GMH) is a pathology that occurs in infancy, with often devastating long-term consequences. Posthemorrhagic hydrocephalus (PHH) can develop acutely, while periventricular leukomalacia (PVL) is a chronic sequala. There are no pharmacological therapies to treat PHH and PVL. We investigated different aspects of the complement pathway in acute and chronic outcomes after murine neonatal GMH induced at postnatal day 4 (P4). Following GMH-induction, the cytolytic complement membrane attack complex (MAC) colocalized with infiltrating red blood cells (RBCs) acutely but not in animals treated with the complement inhibitor CR2-Crry. Acute MAC deposition on RBCs was associated with heme oxygenase-1 expression and heme and iron deposition, which was reduced with CR2-Crry treatment. Complement inhibition also reduced hydrocephalus and improved survival. Following GMH, there were structural alterations in specific brain regions linked to motor and cognitive functions, and these changes were ameliorated by CR2-Crry, as measured at various timepoints through P90. Astrocytosis was reduced in CR2-Crry-treated animals at chronic, but not acute, timepoints. At P90, myelin basic protein and LAMP-1 colocalized, indicating chronic ongoing phagocytosis of white matter, which was reduced by CR2-Crry treatment. Data indicate acute MAC-mediated iron-related toxicity and inflammation exacerbated the chronic effects of GMH.

Cerebral Lateral Ventricular Asymmetry: Normal Variant or an Indicator of Underlying Pathology

Introduction: Isolated lateral ventricular asymmetry has been associated with a favorable prognosis; however, prenatal evaluations in existing studies have been conducted using ultrasonography (US). This study aimed to describe the magnetic resonance imaging (MRI) findings, progression of ventricular asymmetry, and perinatal outcomes in fetuses prenatally diagnosed with isolated ventricular asymmetry. Methods: This retrospective study included patients who underwent MRI for isolated fetal ventricular asymmetry at a tertiary center between January 2012 and January 2020. Information, including pregnancy history, US, MRI findings, and perinatal outcomes, was obtained from medical records. Results: The study cohort included 17 women with fetal ventricular asymmetry but without ventriculomegaly at the time of index US. Mild ventriculomegaly subsequently developed in 13 patients; 12 of them showed spontaneous resolution before delivery. MRI identified low-grade intraventricular hemorrhage (IVH) in 13 fetuses. Postnatally, 12 newborns underwent neonatal cranial US where two of them showed evidence of germinal matrix hemorrhage. Both newborns appeared normal at birth without neonatal complications. Conclusion: MRI identified low-grade IVH in most fetuses with isolated ventricular asymmetry. These fetuses were also likely to develop mild ventriculomegaly with spontaneous resolution. Although perinatal outcomes appeared good, careful follow-up in both prenatal and postnatal periods is warranted.

Neuroimaging of Germinal Matrix and Intraventricular Hemorrhage in Premature Infants.

Germinal matrix and intraventricular hemorrhage (GM-IVH) are the major causes of intracranial hemorrhage in premature infants. Cranial ultrasound (cUS) is the imaging modality of choice for diagnosing and classifying GM-IVH. Magnetic resonance imaging (MRI), usually performed at term-equivalent age, is more sensitive than cUS in identifying hemorrhage in the brain. Post-hemorrhagic ventricular dilatation is a significant complication of GM-IVH and correlates with adverse neurodevelopmental outcomes. In this review, we discuss the various imaging findings of GM-IVH in premature infants, focusing on the role of cUS and MRI.

Cerebral blood flow patterns in preterm and term neonates assessed with pseudo-continuous arterial spin labeling perfusion MRI.

In preterm (PT) infants, regional cerebral blood flow (CBF) disturbances may predispose to abnormal brain maturation even without overt brain injury. Therefore, it would be informative to determine the spatial distribution of grey matter (GM) CBF in PT and full-term (FT) newborns at term-equivalent age (TEA) and to assess the relationship between the features of the CBF pattern and both prematurity and prematurity-related brain lesions. In this prospective study, we obtained measures of CBF in 66 PT (51 without and 15 with prematurity-related brain lesions) and 38 FT newborns through pseudo-continuous arterial spin labeling (pCASL) MRI acquired at TEA. The pattern of GM CBF was characterized by combining an atlas-based automated segmentation of structural MRI with spatial normalization and hierarchical clustering. The effects of gestational age (GA) at birth and brain injury on the CBF pattern were investigated. We identified 4 physiologically-derived clusters of brain regions that were labeled Fronto-Temporal, Parieto-Occipital, Insular-Deep GM (DGM) and Sensorimotor, from the least to the most perfused. We demonstrated that GM perfusion was associated with GA at birth in the Fronto-Temporal and Sensorimotor clusters, positively and negatively, respectively. Moreover, the presence of periventricular leukomalacia was associated with significantly increased Fronto-Temporal GM perfusion and decreased Insular-DGM perfusion, while the presence of germinal matrix hemorrhage appeared to mildly decrease the Insular-DGM perfusion. Prematurity and prematurity-related brain injury heterogeneously affect brain perfusion. ASL MRI may, therefore, have strong potential as a noninvasive tool for the accurate stratification of individuals at risk of domain-specific impairment.

Navigation guidance in neuroendoscopic management of complex hydrocephalus

Patients with multiloculated hydrocephalus have multiple, separate abnormal CSF collections with no communication between them. Causes include complications of neonatal meningitis, germinal matrix hemorrhage in neonates, head trauma, and intracranial surgery. Endoscopic fenestration with shunt insertion is a safe and less invasive technique as the initial treatment. In this video, the authors demonstrate a few cases in which electromagnetic navigation was used with a stylet inserted through the operating endoscope to guide the surgeon. Modalities such as insertion of intraventricular contrast and fluorescein may be used as adjuvants, as demonstrated. The use of navigation helps to identify distorted anatomical landmarks and guides surgery. The video can be found here: https://stream.cadmore.media/r10.3171/2023.1.FOCVID22152.

Prevalence, and Pattern of Hypoxic Ischemic Encephalopathy on Magnetic Resonance Imaging among Pediatric patients

Background: Hypoxic Ischemic Encephalopathy is a frequently encountered occurrence in a pediatric setting and more prevalent in the low middle income countries. Magnetic resonance imaging (MRI) is considered a reliable source of investigation. Our study determined the imaging findings and cause of Hypoxic ischemic encephalopathy in children referred for MR Imaging to our radiology department. Study design: A prospective cross-sectional study. Place and duration of study: Our prospective cross-sectional study was conducted at a pediatric tertiarycare hospital, of Karachi Pakistan from 1st November 2021 to 30th October 2022. Methods: Our study included children from newborns to 16 years of age who either had a history of fits, abnormal APGAR score, delayed cry or delayed milestones. The brain MRI was performed on 1.5 tesla scanner with a standard protocol and interpreted by Experienced Radiologists Findings were recorded on anExcel Sheet and data was analyzed on SPSS version 26. Our study included children from newborns to 16 years of age who were at risk of hypoxic insult and were born to mothers who had hypertension, diabetes milletus, history of maternal substance abuse and maternal history of fits history of fits and children who had a history of fits, abnormal APGAR score, delayed cry and/or delayed milestones. Children who were born via instrumental delivery were excluded from our study. Result: A total number of 187 patients were included in our study with 98 males and 89 females. The most common age group involved was from age >1 year to 5 years (50.3%). The most common presenting complaints included delayed milestones (63.6%) and fits (59.9%), delayed cry (52.4). On examination 42.2% had microcephaly. One-third of the patients had a positive maternal history for diabetes mellitus, hypertension and anemia. APGAR score was checked at 1 minute and 5 minute which showed the most common APGAR score of 3-6 which was seen in 81.8% of the patients. On MR Imaging 54.5% had periventricular leukomalacia, 35.3% had deep gray matter involvement, 3.7% had germinal matrix hemorrhage, and only 1.6% had watershed infarcts. A statically significant association was seen between gestation at birth and periventricular leukomalacia (P=<0.5). Conclusion: Hypoxic Ischemic Encephalopathy is a common occurrence in our society and MRI is the recommended modality due to its sensitivity and superior soft-tissue resolution. In developing countries due to a lack of proper facilities and awareness, there is an increased incidence of HIE which leads to increased morbidity therefore increasing awareness and early diagnosis is of utmost importance. Keywords: Hypoxic ischemic encephalopathy, Magnetic Resonance Imaging, Pediatric population

The Role of Oxidative Stress in the Progression of Secondary Brain Injury Following Germinal Matrix Hemorrhage.

Germinal matrix hemorrhage (GMH) can be a fatal condition responsible for the death of 1.7% of all neonates in the USA. The majority of GMH survivors develop long-term sequalae with debilitating comorbidities. Higher grade GMH is associated with higher mortality rates and higher prevalence of comorbidities. The pathophysiology of GMH can be broken down into two main titles: faulty hemodynamic autoregulation and structural weakness at the level of tissues and cells. Prematurity is the most significant risk factor for GMH, and it predisposes to both major pathophysiological mechanisms of the condition. Secondary brain injury is an important determinant of survival and comorbidities following GMH. Mechanisms of brain injury secondary to GMH include apoptosis, necrosis, neuroinflammation, and oxidative stress. This review will have a special focus on the mechanisms of oxidative stress following GMH, including but not limited to inflammation, mitochondrial reactive oxygen species, glutamate toxicity, and hemoglobin metabolic products. In addition, this review will explore treatment options of GMH, especially targeted therapy.

Imaging the Cerebral Veins in Pediatric Patients: Beyond Dural Venous Sinus Thrombosis.

The range of intracranial venous anomalies in children differs from that in adults. As a commonly encountered highly morbid disease, sinovenous thrombosis has been discussed extensively in the literature, and the associated imaging considerations are similar in pediatric and adult patients. The authors shift the focus to less frequently discussed cerebral venous diseases in pediatric patients. First, the practical embryology pertinent to malformations, syndromes, and variants such as vein of Galen aneurysmal malformation, Sturge-Weber syndrome, and developmental venous anomalies are discussed. Second, anatomic considerations that are applicable to neuroimaging in pediatric patients with cerebral venous anomalies are reviewed. In the discussion of anatomy, special attention is given to the medullary venous system that serves the cerebral white matter, superficial cortical veins (tributaries of the dural venous sinuses), and bridging veins, which carry blood from the superficial cortical veins through the potential subdural space into the dural venous sinuses. Third, the selection of imaging modalities (US, CT and CT venography, and MRI) is addressed, and various MR venographic pulse sequences (time-of-flight, phase-contrast, and contrast-enhanced sequences) are compared. Finally, a broad variety of congenital and acquired superficial and deep venous diseases in children are reviewed, with emphasis on less frequently discussed entities involving the medullary (eg, deep medullary venous engorgement and thrombosis, periventricular hemorrhagic venous infarction due to germinal matrix hemorrhage), cortical (eg, cortical venous thrombosis), and bridging (eg, acute and chronic manifestations of injury in abusive head trauma) veins, as well as the deep veins and dural venous sinuses (eg, varix). © RSNA, 2023 Quiz questions for this article are available through the Online Learning Center. Online supplemental material and the slide presentation from the RSNA Annual Meeting are available for this article.

OBSERVATIONAL STUDY ON ROLE OF NEUROSONOGRAM IN INTRACRANIAL PATHOLOGIES IN NEONATES AT A TERTIARY CARE CENTER.

ABSTRACT BACKGROUND AND OBJECTIVES: Neonates face a lot of challenges especially based on their gestational age, maternal factors, birth weight at the time of delivery, immediate cry following birth. H ypoxic ischemic encephalopathy and Germinal matrix haemorrhage constitutes major portion of those challenges. To identify varied conditions, we can take help of imaging in form of neurosonogram. METHODS : Neurosonogram was carried out on all n tool including followeonates both as screening and diagnostic up scans. A total of 100 preterm babies with positive findings were included in the study. An analysis was performed over different pathologies including grading of specific condition in requir ed areas. RESULTS: Our study comprising of 100 neonates with brain pathologies showed following results. In our study of 100 neonates, most of the disease burden is by vascular causes (56%), then followed by infective (19%), congenit al (14%), trauma (8%), metabolic (2%) and miscellaneous (2%). 52% of PVL showed associated risk factors. CONCLUSION: In our study 100 preterm babies with suspected brain injuries were studied with ultrasound through anterior fontanelle and mastoid sutures. Neurosonogram can detect various intracranial pathologies on par with CT scan . Transcranial doppler can reflect the cerebral blood volume and perfusion status through RESISTIVE INDEX and abnormal values according to literature are >0.8 and <0.4 and can be noticed in severe HIE and conditions which increases intracranial pressure . Any measure that decreases the vasospasm which decreases RI can eventually prevent the neonate having progression of ischemia and further new infarct. 1