Cerebrus

Click "Search" to find an article
GMH/IVH - keywords
GMH and IVH references to germinolysis r e f e r e n c e s n a v i g a t o r Abbott NJ, Rönnbäck L, Hansson E (2006) Astrocyte-endothelial interactions at the blood–brain barrier. Nature reviews Neuroscience, vol 7, 41-53. Adams-Chapman I, Hansen NI, Stoll BJ, et al. Neurodevelopmental outcome of extremely low birth weight infants with posthemorrhagic hydrocephalus requiring shunt insertion. Pediatrics 2008;121:e1167–77.  Adcock K, Hedberg C, Loggins J, et al. The TNF-alpha -308, MCP-1 -2518 and TGF-beta1 +915 polymorphisms are not associated with the development of chronic lung disease in very low birth weight infants. Genes Immun. 2003; 4(6):420–426.  Ancel PY, Goffinet F, and the EPIPAGE-2 Writing Group. Epipage Survival and Morbidity of Preterm Children Born at 22 Through 34 Weeks’ Gestation in France in 2011 Results of the EPIPAGE-2 Cohort Study. JAMA Pediatr. 2015;169(3):230-238. Anstrom JA, Brown WR, Moody DM, Thore CR, Challa VR, Block SM. Subependymal veins in premature neonates: implications for hemorrhage. Pediatr Neurol. 2004;30(1):46-53. Anstrom JA, Thore CR, Moody DM, Challa VR, Block SM, Brown WR. Morphometric assessment of collagen accumulation in germinal matrix vessels of premature human neonates. Neuropathol Appl Neurobiol. 2005 Apr;31(2):181-90. Anström JA, Thore CR, Moody DM, Challa VR Block SM, Brown WR (2005) Histologial analysis of vascular patterns and connections in the ganglionic eminence of prematur neonates. Neuroembryology 3; 4-12.  Anstrom JA, Thore CR, Moody DM, Challa VR, Block SM, Brown WR (2005) Germinal matrix cells associate with veins and a glial scaffold in the human fetal brain. Developmental Brain Research 160; 96-100. Anstrom JA, Thore CR, Moody DM, Brown WR (2007) Immunolocalzation of tight junction proteins in blood vessels in human germinal matrix and cortex. Histochem. Cell Biol 127; 205-213. Armstrong DL, Sauls CD, Goddard-Finegold J. Neuropathologic findings in short-term survivors of intraventricular hemorrhage. Am J Dis Child. 1987;141(6):617-21. Ballabh P, Braun A, Nedergaard M. Anatomic analysis of blood vessels in germinal matrix, cerebral cortex, and white matter in developing infants. Pediatr Res. 2004 Jul;56(1):117-24. Ballabh P, Hu F, Kumarasiri M, Braun A, Nedergaard M. Development of tight junction molecules in blood vessels of germinal matrix, cerebral cortex, and white matter. Pediatr Res. 2005 Oct;58(4):791-8. Ballabh P, Xu H, Hu F, et al. Angiogenic inhibition reduces germinal matrix hemorrhage. Nat Med. 2007; 13(4):477–485.  Ballabh P. Pathogenesis and Prevention of Intraventricular hemorrhage. Clin Perinatol. 2014; 41(1): 47–67. Bassan H, Benson CB, Limperopoulos C, Feldman HA, Ringer SA, Veracruz E, Stewart JE, Soul JS, Disalvo DN, Volpe JJ, du Plessis AJ (2006) Ultrasonographic features and severity scoring of periventricular hemorrhagic infarction in relation to risk factors and outcome. Pediatrics 117:2111-2118.  Bassan H, Limperopoulos C, Visconti K, Mayer DL, Feldman HA, Avery L, Benson CB, Stewart J, Ringer SA, Soul JS, Volpe JJ, du Plessis AJ. Neurodevelopmental outcome in survivors of periventricular hemorrhagic infarction. Pediatrics. 2007;120(4):785-92. Battin MR, Maalouf EF, Counsell SJ, Herlihy AH, Rutherford MA, Azzopardi D, et al. Magnetic resonance imaging of the brain in very preterm infants: visualization of the germinal matrix, early myelination, and cortical folding. Pediatrics. 1998 Jun;101(6):957-62. Bell AH, Miller SL, Castillo-Melendez M, Malhotra A (2020) The neurovascular unit: effects of brain insults during the perinatal period. Frontiers in Neuroscience 13; 1452. Bejar R, Coen RW, Ekpoudia I, James HE, Gluck L (1985) Real time ultrasound diagnosis of hemorrhagic pathological conditions in the posterior fossa of preterm infants. Neurosurgery 16:281–289. Bowerman RA, Donn SM, Silver TM, Jaffe MH. Natural history of neonatal periventricular/intraventricular hemorrhage and its complications: sonographic observations. AJR Am J Roentgenol.1984;143(5):1041-52. Brann BS 4th, Qualls C, Wells L, Papile L. Asymmetric growth of the lateral cerebral ventricle in infants with posthemorrhagic ventricular dilation. J Pediatr. 1991;118(1):108-12. Braun A, Xu H, Hu F, Kocherlakota P, Siegel D, Chander P, et al. Paucity of pericytes in germinal matrix vasculature of premature infants. J Neurosci. 2007 Oct 31;27(44):12012-24. Bravo MC, Lubian S, Horsch S, Cabañas F, de Vries LS; EurUS.Brain group. Neonatal ventriculomegaly: Pathophysiology and management guided with cranial ultrasonography. Dev Med Child Neurol. 2024 Nov;66(11):1419-1431. doi: 10.1111/dmcn.15955. Epub 2024 May 15. PMID: 38747316.Brouwer A, Groenendaal F, van Haastert IL, Rademaker K, Hanlo P, de Vries L. Neurodevelopmental outcome of preterm infants with severe intraventricular hemorrhage and therapy for post-hemorrhagic ventricular dilatation. J Pediatr. 2008;152(5):648-54. Brouwer MJ, de Vries LS, Groenendaal F, Koopman C, Pistorius LR, Mulder EJ, Benders MJ. New reference values for the neonatal cerebral ventricles. Radiology. 2012;262(1):224-33. Brouwer AJ, van Stam C, Uniken Venema M, Koopman C, Groenendaal F, de Vries LS. Cognitive and neurological outcome at the age of 5-8 years of preterm infants with post-hemorrhagic ventricular dilatation requiring neurosurgical intervention. Neonatology. 2012;101(3):210-6. Brouwer AJ, Brouwer MJ, Groenendaal F, Benders MJ, Whitelaw A, de Vries LS. European perspective on the diagnosis and treatment of posthaemorrhagic ventricular dilatation. Arch Dis Child Fetal Neonatal Ed. 2012;97(1):F50-5. Brouwer AJ, Groenendaal F, Benders MJ, de Vries LS. Early and late complications of germinal matrix-intraventricular haemorrhage in the preterm infant: what is new? Neonatology. 2014;106(4):296-303. Brouwer AJ, Groenendaal F, Han KS, de Vries LS. Treatment of neonatal progressive ventricular dilatation: a single-centre experience. J Matern Fetal Neonatal Med. 2015;28 Suppl 1:2273-9. Brown LS, Foster CG, Courtney JM, King NE, Howells DW, Sutherland BA (2019) Pericytes and Neurovascular Function in the Healthy and Diseased Brain. Front. Cell. Neurosci., 28 June 2019 | https://doi.org/10.3389/fncel.2019.00282 Brown WD, Gerfen GW, Vachon LA, Nelson MD (1994) Real-time ultrasonography of arterial IVH in preterm infants. Pediatric Neurology 11:325–327. Camfferman FA, Govaert P, Groenendaal F, Vanderhasselt T, Cools F, Dudink J. Internal Cerebral Vein Doppler Velocities Reflect Maturational Changes and Hemorrhage Risk in Preterm Infants. AJNR Am J Neuroradiol. 2026 May 7.  Camfferman FA, Govaert P, Lequin MH, Groenendaal F, Tataranno ML, KizilatesU, Benders MJNL, Dudink J. Toward a Broader Classification of Deep Venous Cerebral Anatomy in Extremely Preterm Infants: A Literature-Based Approach andIts Relevance to Intraventricular Hemorrhage. AJNR Am J Neuroradiol. 2026 Feb 3;47(2):496-502. Carteaux P, Cohen H, Check J, George J, McKinley P, Lewis W, Hegwood P, Whitfield JM, McLendon D, Okuno-Jones S, Klein S, Moehring J, McConnell C (2003) Evaluation and development of potentially better practices for the prevention of brain hemorrhage and ischemic brain injury in very low birth weight infants. Pediatrics 111:e489-96. Chen Z, Gao C, Hua Y, Keep RF, Muraszko K, Xi G. Role of iron in brain injury after intraventricular hemorrhage. Stroke. 2011;42:465-70. Corbin JG, Gaiano N, Juliano SL, Poluch S, Stancik E, Haydar TF. Regulation of neural progenitor cell development in the nervous system. J Neurochem. 2008 Sep;106(6):2272-87. Counsell SJ, Maalouf EF, Rutherford MA, Edwards AD (1999) Periventricular haemorrhagic infarct in a preterm neonate. Eur J Paediatr Neurol 3:25-7. Darrow VC, Alvord EC jr, Mack LA, Hodson WA (1988) Histologic evolution of the reactions to hemorrhage in the premature human infant’s brain. A combined ultrasound and autopsy study and a comparison with the reaction in adults. Am J Pathol 130:44-58. Davies MW, Swaminathan M, Chuang SL, Betheras FR. Reference ranges for the linear dimensions of the intracranial ventricles in preterm neonates. Arch Dis Child Fetal Neonatal Ed. 2000;82(3):F218-23. Davis AS, Hintz SR, Goldstein RF, Ambalavanan N, Bann CM, Stoll BJ, Bell EF, Shankaran S, Laptook AR, Walsh MC, Hale EC, Newman NS, Das A, Higgins RD; Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network. Outcomes of extremely preterm infants following severe intracranial hemorrhage. J Perinatol. 2014;34(3):203-8.  Dawes WJ, Zhang X, Fancy SPJ, Rowitch D, Marino S (2016) Moderate-grade germinal matrix haemorrhage activates cell division in the neonatal mouse subventricular zone. Dev Neurosci 38; 430-444. Debus O, Koch HG, Kurlemann G, et al. Factor V Leiden and genetic defects of thrombophilia in childhood porencephaly. Arch Dis Child Fetal Neonatal Ed. 1998; 78(2):F121–124.  Del Bigio MR. Cell proliferation in human ganglionic eminence and suppression after prematurity-associated haemorrhage. Brain 2011;134:1344–61. Dempsey EM, Barrington KJ. Treating hypotension in the preterm infant: when and with what: a critical and systematic review. J Perinatol 2007;27:469–78.  De Vries LS, Groenendaal F, van Haastert IC, Eken P, Rademaker KJ, Meiners LC (1999) Asymmetrical myelination of the posterior limb of the internal capsule in infants with periventricular haemorrhagic infarction: an early predictor of hemiplegia. Neuropediatrics 30(6):314-9. De Vries LS, Groenendaal F, Gooskens R, Hanlo P. Unilateral posthaemorrhagic hydrocephalus in the neonatal period or later in infancy. Acta Paediatr. 2000;89(1):77-81.  de Vries LS, Roelants-van Rijn AM, Rademaker KJ, Van Haastert IC, Beek FJ, Groenendaal F (2001) Unilateral parenchymal haemorrhagic infarction in the preterm infant. Eur J Paediatr Neurol 5:139-49. Dewbury KC, Bates RI. Neonatal intracranial haemorrhage: the cause of the ultrasound appearances. Br J Radiol. 1983;56(671):783-9.  Dolfin T, Skidmore MB, Fong KW, Hoskins EM, Shennan AT (1983) Incidence, severity, and timing of subependymal and intraventricular hemorrhages in preterm infants born in a perinatal unit as detected by serial real-time ultrasound. Pediatrics 71(4):541-6. Donn SM, Bowerman RA. Neonatal posthemorrhagic porencephaly. Ultrasonographic features. Am J Dis Child 1982; 36:707-709. Dudink J, Lequin M, Weisglas-Kuperus N, Conneman N, van Goudoever JB, Govaert P. Venous subtypes of preterm periventricular haemorrhagic infarction. Arch Dis Child Fetal Neonatal Ed. 2008;93(3):F201-6. El-Khoury N, Braun A, Hu F, Pandey M, Nedergaard M, Lagamma EF, et al. Astrocyte end-feet in germinal matrix, cerebral cortex, and white matter in developing infants. Pediatr Res. 2006 May;59(5):673-9. EXPRESS Group, Fellman V, Hellström-Westas L, Norman M, Westgren M, Källén K, Lagercrantz H, Marsál K, Serenius F, Wennergren M. One-year survival of extremely preterm infants after active perinatal care in Sweden. JAMA. 2009 Jun 3;301(21):2225-33 Fleischer AC, Hutchison AA, Allen JH, Stahlman M, Meacham WF, James AE (1981) The role of sonography and the radiologist–ultrasonologist in the detection and follow-up of intracranial hemorrhage in the preterm neonate. Radiology 139:733–736. Fowlie PW, Davis PG, McGuire W. Prophylactic intravenous indomethacin for preventing mortality and morbidity in preterm infants. Cochrane Database Syst Rev. 2010; (7):CD000174. Funato M, Tamai H, Takeda Z (1994) Moment of intraventricular hemorrhage—clinical pathogenic events. In: Lou, H.C., Greisen, G., Larsen, J.F. (Eds.) Brain Lesions in the Newborn. Hypoxic and Haemodynamic Pathogenesis. Alfred Benzon Symposium No. 37. Munksgaard, pp. 456–469. Ghazi-Birry H, Brown W, Moody D, Challa V, Block S, and Reboussin D (1977) Human Germinal Matrix: Venous Origin of Hemorrhage and Vascular Characteristics. Am J Neuroradiol 18:219-229. Golden JA, Gilles FH, Rudelli R, Leviton A. Frequency of neuropathological abnormalities in very low birth weight infants. J Neuropathol Exp Neurol. 1997;56(5):472-8. Gopel W, Hartel C, Ahrens P, et al. Interleukin-6-174-genotype, sepsis and cerebral injury in very low birth weight infants. Genes Immun. 2006; 7(1):65–68.  Gould SJ, Howard S, Hope PL, Reynolds EOR (1986) Periventricular intraparenchymal cerebral haemorrhage in preterm infants: the role of venous infarction. J Pathol 151:197–202. Govaert P, Smets K, Matthys E, Oostra A (1999) Neonatal focal temporal lobe or atrial wall haemorrhagic infarction. Arch Dis Child Fetal Neonatal Ed 81(3):F211-6. Govaert P, De Vries LS. An atlas of neonatal brain sonography, 2nd ed. London, England: Mac Keith Press, 2010:199-224. Govaert P, Triulzi F, Dudink J (2020) The developing brain by trimester. Handb Clin Neurol 171:245-289. Gram M, Sveinsdottir S, Ruscher K, Hansson SR, Cinthio M, Akerström B, Ley D. Hemoglobin induces inflammation after preterm intraventricular hemorrhage by methemoglobin formation. J Neuroinflammation. 2013 ;10:100. Grant EG, Kerner M, Schellinger O, et al. Evolution of porencephalic cysts from intraparenchymal hemorrhage in neonates. Sonographic evidence. AJNR 1982;3:47-50, AiR 1982; 138:467-470. Grant EG, White EM (1986) Pediatric neurosonography. J Child Neurol 1:319–337. Greisen G. Autoregulation of cerebral blood flow in newborn babies. Early Hum Dev. 2005;81:423-28. Gressens P, Richelme C, Kadhim HJ, Gadisseux JF, Evrard P. The germinative zone produces the most cortical astrocytes after neuronal migration in the developing mammalian brain. Biol Neonate 1992;62:4-24.  Guzzetta F, Shackelford GD, Volpe S, Perlman JM, Volpe JJ. Periventricular intraparenchymal echodensities in the premature newborn: critical determinant of neurologic outcome. Pediatrics. 1986;78(6):995-1006. Habas PA, Kim K, Corbett-Detig JM, Rousseau F, Glenn OA, Barkovich AJ, et al. A spatiotemporal atlas of MR intensity, tissue probability and shape of the fetal brain with application to segmentation. Neuroimage. 2010 Nov 1;53(2):460-70. Hambleton G, Wigglesworth JS. Origin of intraventricular haemorrhage in the preterm infant. Arch Dis Child. 1976;51(9):651-9. Harteman JC, Groenendaal F, van Haastert IC, et al. Atypical timing and presentation of periventricular haemorrhagic infarction in preterm infants: the role of thrombophilia. Developmental Med Child Neurol. 2012; 54(2):140–147.  Hope PL, Gould SJ, Howard S, Hamilton PA, Costello AM, Reynolds EO. Precision of ultrasound diagnosis of pathologically verified lesions in the brains of very preterm infants. Dev Med Child Neurol. 1988; 30(4):457-71. Horbar JD, Carpenter JH, Badger GJ, Kenny MJ, Soll RF, Morrow KA, Buzas JS. Mortality and neonatal morbidity among infants 501 to 1500 grams from 2000 to 2009. Pediatrics. 2012;129(6):1019-26.  Horsch S, Kutz P, Roll C. Late germinal matrix hemorrhage-like lesions in very preterm infants. J Child Neurol. 2010;25(7):809-14. Kent T, Sinha V, Ceyhan E, et al. Deep cerebral venous abnormalities in premature babies with GMH-IVH: a single-centre retrospective study. BMJ Paediatr Open 2023;7. Kersbergen KJ, Groenendaal F, Benders MJ, van Straaten HL, Niwa T, Nievelstein RA, de Vries LS. The spectrum of associated brain lesions in cerebral sinovenous thrombosis: relation to gestational age and outcome. Arch Dis Child Fetal Neonatal Ed. 2011;96(6):F404-9.  Kinoshita Y, Okudera T, Tsuru E, Yokota A (2001) Volumetric Analysis of the Germinal Matrix and Lateral Ventricles Performed Using MR Images of Postmortem Fetuses. Am J Neuroradiol 22:382–388. Kirks DR, Bowie JD (1986) Cranial ultrasonography of neonatal periventricular/intraventricular hemorrhage: who, how, why and when? Pediatric Radiol 16:114–119. Klebermass-Schrehof K, Czaba C, Olischar M, Fuiko R, Waldhoer T, Rona Z, Pollak A, Weninger M. Impact of low-grade intraventricular hemorrhage on long-term neurodevelopmental outcome in preterm infants. Childs Nerv Syst. 2012;28(12):2085-92. Kluckow M, Evans N, Osborn D. Low Systemic Blood Flow and Brain injury in the Preterm Infant. Neoreviews 2004; 5(3): e98–108.  Koumanidou C, Vakaki M, Anagnostara A, Pitsoulakis G, Kakavakis K, Mirilas P. Hemorrhage in the cavum septi pellucidi, and a brief review of the literature. Neuroradiology. 2002 ;44(9):770-4. Kuban K, Teele RL (1984) Rationale for grading intracranial hemorrhage in premature infants. Pediatrics 74:358–363.  Larroche J-Cl (1977) Developmental pathology of the neonate.North-Holland: Elsevier. Larroque B, Marret S, Ancel PY, Arnaud C, Marpeau L, Supernant K, Pierrat V, Rozé JC, Matis J, Cambonie G, Burguet A, Andre M, Kaminski M, Bréart G; EPIPAGE Study Group. White matter damage and intraventricular hemorrhage in very preterm infants: the EPIPAGE study. J Pediatr. 2003;143(4):477-83. LeFlore JL, Broyles RS, Pritchard MA, Engle WD (2003) Value of neurosonography in predicting subsequent cognitive and motor development in extremely low birth weight neonates. J Perinatol 23:629-34. Leijser LM, Miller SP, van Wezel-Meijler G, Brouwer AJ, Traubici J, van Haastert IC, Whyte HE, Groenendaal F, Kulkarni AV, Han KS, Woerdeman PA, Church PT, Kelly EN, van Straaten HLM, Ly LG, de Vries LS. Posthemorrhagic ventricular dilatation in preterm infants: When best to intervene? Neurology. 2018 ;90(8):e698-e706. Levene MI, Starte DR. A longitudinal study of post-haemorrhagic ventricular dilatation in the newborn. Arch Dis Child. 1981;56(12):905-10. Levene MI. Measurement of the growth of the lateral ventricles in preterm infants with real-time ultrasound. Arch Dis Child. 1981;56(12):900-4. Leviton A, Pagano M, Kuban KC, Krishnamoorthy KS, Sullivan KF, Allred EN. The epidemiology of germinal matrix hemorrhage during the first half-day of life. Dev Med Child Neurol. 1991;33(2):138-45. Ley D, Romantsik O, Vallius S, Sveinsdóttir K, Sveinsdóttir S, Agyemang AA, Baumgarten M, Mörgelin M, Lutay N, Bruschettini M, Holmqvist B, Gram M. High Presence of Extracellular Hemoglobin in the Periventricular White Matter Following Preterm Intraventricular Hemorrhage. Front Physiol. 2016;7:330. Maitre NL, Marshall DD, Price WA, Slaughter JC, O'Shea TM, Maxfield C, Goldstein RF. Neurodevelopmental outcome of infants with unilateral or bilateral periventricular hemorrhagic infarction. Pediatrics. 2009;124(6):e1153-60. Marin-Padilla M (1996) Developmental neuropathology and impact of perinatal brain damage. I : Hemorrhagic lesions of neocortex. J Neuropath Exp Neurol 55:758-773. Miletin J, Dempsey EM. Low superior vena cava flow on day 1 and adverse outcome in the very low birthweight infant. Arch Dis Child Fetal Neonatal Ed 2008;93:F368–F371  Meek JH, Tyszczuk L, Elwell CE, Wyatt JS (1999) Low cerebral blood flow is a risk factor for severe intraventricular haemorrhage. Arch Dis Child Fetal Neonat Ed 81, F15-F18 Ment LR, Stewart WB, Ardito TA, Huang E, Madri JA. Indomethacin promotes germinal matrix microvessel maturation in the newborn beagle pup. Stroke. 1992 Aug;23(8):1132-7. Ment LR, Vohr BR, Makuch RW, et al. Prevention of intraventricular hemorrhage by indomethacin in male preterm infants. J Pediatr. 2004; 145(6):832–834.  Moody DM, Brown WR, Challa VR, Block SM (1994) Alkaline phosphatase histochemical staining in the study of germinal matrix hemorrhage and brain vascular morphology in a very-low-birth-weight neonate. Pediatr Res 35:424-430. Murphy BP, Inder TE, Rooks V, Taylor GA, Anderson NJ, Mogridge N, Horwood LJ, Volpe JJ. Posthaemorrhagic ventricular dilatation in the premature infant: natural history and predictors of outcome. Arch Dis Child Fetal Neonatal Ed. 2002;87(1):F37-41.  Nadeem T, Bommareddy A, Bolarinwa L, Cuervo H (2022) Pericyte dynamics in the mouse germinal matrix angiogenesis. Faseb Journal 2022;36:e22339. Nakamura Y, Okudera T, Fukuda S, Hashimoto T (1990) Germinal matrix hemorrhage of venous origin in preterm neonates. Human Pathol 21:1059-1062. Nakamura Y, Okudera T, Hashimoto T (1991) Microvasculature in germinal matrix layer : its relationship to germinal matrix hemorrhage. Modern Pathol 4:475-480. Okudera T, Huang YP, Fukusumi A, Nakamura Y, Hatazawa J, Uemura K (1999) Micro-angiographical studies of the medullary venous system of the cerebral hemisphere. Neuropathology 19:93-111. Osborn DA, Evans N, Kluckow M (2003) Hemodynamic and antecedent risk factors of early and late periventricular/intraventricular hemorrhage in premature infants. Pediatrics 112:33-9. Ozduman K, Pober BR, Barnes P, Copel JA, Ogle EA, Duncan CC, Ment LR. Fetal stroke. Pediatr Neurol. 2004;30(3):151-62. Padget DH (1956) The cranial venous system in man in reference to development, adult configuration, and relation to the arteries. Am J Anat 98:307-356 Paneth N, Rudelli R, Kazam E, Monte W (1994) Brain Damage in the Preterm Infant. Clinics in Developmental Medicine No. 131. London: Mac Keith Press. Pape KE, Wigglesworth JS (1979) Haemorrhage, Ischaemia and the Perinatal Brain. Clinics in Developmental Medicine No. 69/70. London: Spastics International Medical Publications. Papile LA, Burstein J, Burstein R, Koffler H (1978) Incidence and evolution of subependymal and intraventricular hemorrhage: a study of infants with birth weights less than 1,500 gm. J Pediatr 92(4):529-34.  Parodi A, Morana G, Severino MS, Malova M, Natalizia AR, Sannia A, Rossi A, Ramenghi LA (2013) Low-grade intraventricular hemorrhage: is ultrasound good enough ? J Maternal Fetal Neonatal Medicine  Patra K, Wilson-Costello D, Taylor HG, Mercuri-Minich N, Hack M. Grades I-II intraventricular hemorrhage in extremely low birth weight infants: effects on neurodevelopment. J Pediatr. 2006;149(2):169-73. Perlman JM, Volpe JJ. Intraventricular hemorrhage in extremely small premature infants. Am J Dis Child. 1986;140(11):1122-4. Perlman JM, Rollins N, Burns D, Risser R (1993) Relationship between periventricular intraparenchymal echodensities and germinal matrix–intraventricular hemorrhage in the very low birth weight neonate. Pediatrics 91:474–480. Pierrat V, Duquennoy C, van Haastert IC, Ernst M, Guilley N, de Vries LS. Ultrasound diagnosis and neurodevelopmental outcome of localised and extensive cystic periventricular leukomalacia. Arch Dis Child Fetal Neonatal Ed 2001;84:F151–F156.  Pryds O, Greisen G, Lou H, Friis-Hansen B. Heterogeneity of cerebral vasoreactivity in preterm infants supported by mechanical ventilation. J Pediatr. 1989;115(4): 638–45. Rabe H, Diaz-Rossello JL, Duley L, Dowswell T. Effect of timing of umbilical cord clamping and other strategies to influence placental transfusion at preterm birth on maternal and infant outcomes. Cochrane Database Syst Rev. 2012;8:CD003248. Rademaker KJ, Groenendaal F, Jansen GH, Eken P, de Vries LS (1994) Unilateral haemorrhagic parenchymal lesions in the preterm infant: shape, site and prognosis. Acta Paediatr 83:602–608. Raets MM, Dudink J, Govaert P. Neonatal disorders of germinal matrix. J Matern Fetal Neonatal Med. 2015;28 Suppl 1:2286-90. Ramenghi LA, Gill BJ, Tanner SF, Martinez D, Arthur R, Levene MI (2002) Cerebral venous thrombosis, intraventricular haemorrhage and white matter lesions in a preterm newborn with factor V (Leiden) mutation. Neuropediatrics 33:97-9. Ramenghi LA, Mosca F, Counsell S, Rutherford MA. Magnetic Resonance Imaging of the Brain in Preterm Infants. In: Tortori-Donati P. Pediatric Neuroradiology. Volume 1 (Brain). 1st ed. Berlin, Germany: Springer-Verlag, 2005:199-234. Ramenghi LA, Fumagalli M, Righini A, Triulzi F, Kustermann A, Mosca F. Thrombophilia and fetal germinal matrix-intraventricular hemorrhage: does it matter? Ultrasound Obstet Gynecol. 2005;26(5):574-6. Ramenghi LA, Fumagalli M, Groppo M, Consonni D, Gatti L, Bertazzi PA, Mannucci PM, Mosca F. Germinal matrix hemorrhage: intraventricular hemorrhage in very-low-birth-weight infants: the independent role of inherited thrombophilia. Stroke. 2011;42(7):1889-93. Reeder JD, Kaude JV, Setzer ES (1982) Choroid plexus hemorrhage in premature neonates: recognition by sonography. Am J Neuroradiol 3:619–622. Rhine W, Blankenberg FG. Cranial Ultrasonography. NeoReviews 2001 2(1): 3–11.  Rypens F, Avni EF, Dussaussois L, David P, Vermeylen D, Van Bogaert P, Matos C (1994) Hyperechoic thickened ependyma: sonographic demonstration and significance in neonates. Pediatr Radiol 24:550–553. Rademaker KJ, Groenendaal F, Jansen GH, Eken P, de Vries LS (1994) Unilateral haemorrhagic parenchymal lesions in the preterm infant: shape, site and prognosis. Acta Paediatr 83(6):602-8.  Rademaker KJ, Govaert P, Vandertop WP, Gooskens R, Meiners LC, de Vries LS. Rapidly progressive enlargement of the fourth ventricle in the preterm infant with post-haemorrhagic ventricular dilatation. Acta Paediatr. 1995;84(10):1193-6. Robinson S. Neonatal posthemorrhagic hydrocephalus from prematurity: pathophysiology and current treatment concepts. J Neurosurg Pediatr. 2012;9(3):242-58. Roelants-van Rijn AM, Groenendaal F, Beek FJ, Eken P, van Haastert IC, de Vries, LS (2001) Parenchymal brain injury in the preterm infant: comparison of cranial ultrasound, MRI and neurodevelopmental outcome. Neuropediatrics 32:80-9. Roze E, Benders MJ, Kersbergen KJ, van der Aa NE, Groenendaal F, van Haastert IC, Leemans A, de Vries LS. Neonatal DTI early after birth predicts motor outcome in preterm infants with periventricular hemorrhagic infarction. Pediatr Res. 2015;78(3):298-303. Rushton DI, Preston PR, Durbin GM (1985) Structure and evolution of echo dense lesions in the neonatal brain. A combined ultrasound and necropsy study. Arch Dis Child 60:798–808. Rypens E, Avni EF, Dussaussois L, David P, Vermeylen D, van Bogaert P, Matos C. Hyperechoic thickened ependyma: sonographic demonstration and significance in neonates. Pediatr Radiol. 1994;24(8):550-3.  Sannia A, Natalizia AR, Parodi A, Malova M, Fumagalli M, Rossi A, Ramenghi LA. Different gestational ages and changing vulnerability of the premature brain. J Matern Fetal Neonatal Med. 2015; 28 Suppl 1:2268-72. Saunders NR, Dziegielewska KM, Mollgard K, Habgood MD (2018). Physiology and molecular biology of barrier mechanisms in the fetal and neonatal brain. J. Physiol. 596, 5723–5756. Schmidt H (1965) Untersuchungen zur Pathogenese und Ätiologie der geburtstraumatischen Hirnschädigungen Früh- und Reifgeborener. Jena: Gustav Fisher Verlag. Schwartz P (1961) Birth Injuries of the Newborn. Basel/New York: Karger. Scott JA, Habas PA, Kim K, et al. Growth trajectories of the human fetal brain tissues estimated from 3D reconstructed in utero MRI. Int J Dev Neurosci 2011;29:529–36. Shackelford GD, Volpe JJ. Cranial ultrasonography in the evaluation of neonatal intracranial hemorrhage and its complications. J Perinat Med. 1985;13(6):293-304. Shaver DC, Bada HS, Korones SB, Anderson GD, Wong SP, Arheart KL. Early and late intraventricular hemorrhage: the role of obstetric factors. Obstet Gynecol. 1992;80(5):831-7. Sheehan JW, Pritchard M, Heyne RJ, Brown LS, Jaleel MA, Engle WD, Burchfield PJ, Brion LP. Severe intraventricular hemorrhage and withdrawal of support in preterm infants. J Perinatol. 2017;37(4):441-447. Slovis TL, Shankaran S (1984) Ultrasound in the evaluation of hypoxic–ischemic injury and intracranial hemorrhage in neonates: the state of the art. Pediatr Radiol 14:67–75. Stein RL, Rosenbaum AE. Deep supratentorial veins. Section I. Normal deep cerebral venous system. In: Newton TH, Potts DG, eds. Radiology of the Skull and Brain. St. Louis: Mosby; 1974:1903–1998. Steinsmo Ødegård S, Jarmund AH, Pedersen SA, Govaert P, Dudink J, Nyrnes SA. A scoping review of variations in cerebral Doppler venous waveforms in infants. Neuroimage. 2026 Mar;328:121766. Stoll BJ, Hansen NI,Bell EF,et al; Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network. Neonatal outcomes of extremely preterm infants from the NICHD Neonatal Research Network. Pediatrics. 2010;126(3):443-456.  Supramaniam V, Vontell R, Srinivasan L, Wyatt-Ashmead J, Hagberg H, Rutherford M. Microglia activation in the extremely preterm human brain. Pediatr Res. 2013 ;73(3):301-9. Tajdar M, Orlando C, Casini A, Herpol M, De Bisschop B, Govaert P, Neerman-Arbez M, Jochmans K. Heterozygous FGA p.Asp473Ter (fibrinogen Nieuwegein) presenting as antepartum cerebral thrombosis.Thromb Res. 2017 Oct 28. pii: S0049-3848(17)30536-4. Takashima S, Tanaka K (1978) Microangiography and vascular permeability of the subependymal matrix in the premature infant. Can J Neurol Sci 5(1):45-50.  Takashima S, Mito T, Ando Y (1986) Pathogenesis of periventricular white matter hemorrhages in preterm infants. Brain Develop 8:25–30. Taoka T, Fukusumi A, Miyasaka T, et al. Structure of the Medullary Veins of the Cerebral Hemisphere and Related Disorders. Radiographics : a review publication of the Radiological Society of North America, Inc 2017;37:281–297. Tarnow-Mordi W, Morris J, Kirby A et al. Delayed versus Immediate Cord Clamping in Preterm Infants. N Engl J Med. 2017;377(25):2445-2455. Taylor GA. Effect of germinal matrix hemorrhage on terminal vein position and patency. Pediatr Radiol 1995; 25:Suppl 1 S37-40. Toft PB, Leth H, Peitersen B, Lou HC. Metabolic changes in the striatum after germinal matrix hemorrhage in the preterm infant. Pediatr Res. 1997;41(3):309-16. Tortora D, Severino M, Malova M, Parodi A, Morana G, Sedlacik J, Govaert P, Volpe JJ, Rossi A, Ramenghi LA. Differences in subependymal vein anatomy may predispose preterm infants to GMH-IVH. Arch Dis Child Fetal Neonatal Ed. 2018;103(1):F59-F65.  Tortora D, Martinetti C, Severino M, Uccella S, Malova M, Parodi A, Brera F, Morana G, Ramenghi LA, Rossi A. The effects of mild germinal matrix-intraventricular haemorrhage on the developmental white matter microstructure of preterm neonates: a DTI study. Eur Radiol. 2017 Sep 27. Tortora D, Severino M, Malova M, Parodi A, Morana G, Ramenghi LA, Rossi A. Variability of Cerebral Deep Venous System in Preterm and Term Neonates Evaluated on MR SWI Venography. AJNR Am J Neuroradiol. 2016 Jul 28. Ulfig N. Ganglionic eminence of the human fetal brain--new vistas. Anat Rec. 2002 Jul 1;267(3):191-5. Van Wezel-Meijler G. Neonatal cranial ultrasonography. 1st ed. Berlin, Germany: Springer-Verlag, 2007:53.  Vasileiadis GT, Gelman N, Han VK, Williams LA, Mann R, Bureau Y, et al. Uncomplicated intraventricular hemorrhage is followed by reduced cortical volume at near term age. Pediatrics. 2004;114:e367-72.  Verbeek E, Meuwissen ME, Verheijen FW, Govaert PP, Licht DJ, Kuo DS, et al. COL4A2 mutation associated with familial porencephaly and small-vessel disease. Eur J Hum Genet. 2012 Aug;20(8):844-51. Vinukonda G, Dummula K, Malik S, et al. Effect of prenatal glucocorticoids on cerebral vasculature of the developing brain. Stroke. 2010; 41(8):1766–1773. Volpe JJ. Brain injury in the premature infant: overview of clinical aspects, neuropathology, and pathogenesis. Semin Pediatr Neurol. 1998;5(3):135-51. Volpe JJ (1989) Intraventricular hemorrhage and brain injury in the premature infant. Neuropathology and pathogenesis. Clinics Perinatol 16:361–411. Volpe JJ (1990) Brain injury in the premature infant: is it preventable? Pediatr Res 27:S28–S33. Volpe JJ. Neurology of the Newborn. 5th ed. Philadelphia, PA: Saunders Elsevier, 2008:517-88. Wang J, Wang J, Sun J, et al. Evaluation of the anatomy and variants of internal cerebral veins with phase-sensitive MR imaging. Surg Radiol Anat 2010;32:669–674. Wapner RJ. Antenatal corticosteroids for periviable birth. Semin Perinatol. 2013;37(6):410-3. Whitelaw A. Intraventricular haemorrhage and posthaemorrhagic hydrocephalus: pathogenesis, prevention and future interventions. Semin Neonatol. 2001;6(2):135-46. Xu H, Hu F, Sado Y, et al. Maturational changes in laminin, fibronectin, collagen IV, and perlecan in germinal matrix, cortex, and white matter and effect of betamethasone. J Neurosci Res. 2008; 86(7):1482–1500.  < Altman and bayer 2015: matrix pockets at GA 24w The origin is most often not in sinusoidal capillaries, but rather in the venules of the exterior matrix stratum, where the medullary veins converge. Having been provoked, haemorrhage grows due to weak clotting, or to cerebral hyperperfusion and congestion accompanying pneumothorax, seizures or hypercapnia. Although it is not exceptional to find thrombosis in the smaller veins around and inside a matrix bleed, this does not appear to be the primary event. After bleeding, tissue reaction takes place with invasion by macrophages and astrogliosis. The primary haemorrhage (with a pool of 2–30 mm diameter) regresses with transient cavitation. posthaemorrhagic ventriculomegaly matrix site haemorrhage grading GMH versus germinolysis ultrasound description clinical presentation congestion typical GMH scans GMH/IVH management matrix volume matrix fragility > parenchymal infarction veins After the majority of cortical neurons have formed (by the 16th gestational week), a network of microsize blood vessels (without a muscular wall) persists in a cluster of (sub)ventricular neuroepithelial cells in the wall of the lateral ventricle. This cluster is referred to as ‘germinal matrix’. Vascular rupture inherent to GMH (germinal matrix haemorrhage) occurs at the level of the capillaro-venous transition. Neuroepithelium also resides in the roof of the fourth ventricle, where autopsies reveal haemorrhage in one out of ten cases of preterm intraventricular haemorrhage (IVH). IVH at term mostly originates in choroid plexus, not in germinal matrix. In the preterm the opposite applies, about 90% originates in matrix. Video recording of ultrasound established two variants of GMH (Funato et al. 1994): (1) the rapidly progressive type, maturing within seconds in deeper matrix layers, is immediately hyperechoic and usually presents with a catastrophic clinical picture; (2) the slowly progressive variant, less frequent, takes minutes to become visible in the surface layers of the matrix and is initially hypoechoic. In the first type one may find an island of parenchyma surrounded by blood.  The on-line observation of bleeding into GM has illustrated an arterial jet to the lesion, suggesting the bleeding vessel cannot be distant from feeding arteries (Brown et al. 1994). This hypothesis is challenged by the observation of arterial pulsation in the internal cerebral vein of some preterms with significant ductus arterious L-R shunt, suggesting veins may pulsate in some conditions. Adjacent choroidal arteries may also confer pulsatility to veins.  typical IVH scans GMH/IVH context: matrix and vessels postmortem aspects 24w mixture ——> typical limited limited infarction fresh bilateral large left extensive posterior left GMH -> posterior fossa terminal vein infarction GMH in ultrasound patent collector vein GMH, day 6 cavitating Postnatal GMH-IVH and PHI occur nearly exclusively during the first week of life. In at least 50% of affected infants the onset of GMH-IVH is on the first day of life, and by 72 hours approximately 90% of the lesions can be identified. Progression of GMH-IVH to severe grades occurs rapidly, within 1-3 days (Dolfin et al. 1983, Perlman and Volpe 1986, Leviton et al. 1991, Shaver et al. 1992, Rhine and Blankenberg 2001).   It is striking that premature infants are relatively immune to haemorrhage after the first week of life, irrespectively of gestational age. Reduced vulnerability after the first few days might be related to an increase in tissue oxygen concentration after birth, suppressing VEGF and angiopoetin-2 levels. A shutdown in angiogenesis after birth would induce maturation of vessels making them resistant to rupture (Ballabh et al. 2007 and 2014). If such shutdown occurs, the effect on total matrix pool is unknown. Antenatal GMH-IVH is not uncommon (Ozduman et al. 2004, Ramenghi et al. 2005). An ultrasound scan on admission allows pre-existing brain injury to be identified. If antenatal GMH-IVH occurred well before birth, residual findings (such as ventricular dilatation,  intraventricular clots or strands, parenchymal defects) may be subtle. Venous infarction related to GMH (or not) with an atypical time of onset (antenatal or after 96h when unrelated to a clinical deterioration) has been associated with the presence of thrombophilic disorders, especially factor V Leiden (Harteman et al. 2012). risk factors GMH/IVH clinical presentation Despite remarkable improvement in the care of very preterm infants, germinal matrix-intraventricular hemorrhage (GMH-IVH) and parenchymal haemorrhagic infarction (PHI) remain feared complications in. The risk of GMH-IVH increases with decreasing gestational age: in surviving infants born at 24 weeks of gestation the incidence of the most severe lesions (i.e. grade III GMH-IVH and PHI) ranges between 10-25%, while in surviving infants born beyond 28 weeks grade III GMH-IVH and PHI are diagnosed in less than 5% (Volpe 2008, Express group 2009, Stoll et al. 2010, Ancel et al. 2015).  GMH-IVH is rarely observed beyond 32 week gestation: in such context, especially with a late postnatal onset, GMH-IVH is an epiphenomenon of other diseases like venous thrombosis (Ramenghi et al. 2002, Kersbergen et al. 2011, Tajdar et al. 2017). Manifest hypoxia or abrupt fluctuations in arterial or venous blood pressure cause mechanical rupture of frail matrix vessel walls. Asphyxia and respiratory distress are the two main risk factors for GMH. In a number of babies venous congestion during labour may contribute to the phenomenon. Vaginal breech delivery is an accepted risk factor in preterm infants of less than 34 weeks gestation, and sometimes explains early GMH (onset within six hours after birth). Being outborn was a questionable risk factor.  Evidence suggests that the use of surfactant and prenatal lung ripening with steroids may have reduced the risk by 50 % or more. First day indomethacin administration accelerates matrix vessel maturation and reduces the risk of bleeding, but is not recommended because long-term benefit of such strategy has not been demonstrated.  Most occurrences of GMH-IVH/PHI are clinically silent and detected incidentally by routine cranial ultrasound examination or aEEG observations. Some infants manifest with subtle abnormalities in the level of consciousness, movement, tone and eye movement in the hours to days after the IVH. GMH-IVH and PHI can be accompanied by various degrees of cardiorespiratory instability and anaemia. In the most severe cases a catastrophic deterioration may occur with stupor, coma, decerebrate posturing, generalised tonic seizures or hypotonia (Volpe 2008). Laminin, type IV collagen and heparin sulphate proteoglycan perlecan form the basal lamina of brain vessels. Together with the basal lamina, fibronectin, present in extracellular matrix, also plays a role in structural stability. Xu et al. 2008 found that fibronectin levels in GM were significantly lower than WM or cerebral cortex. Fibronectin levels in WM and cortex increased significantly with advancing GA, but not in GM.  The expression of type IV collagen chains and perlecan are not different between cortex, WM or GM (Anstrom et al. 2005). Laminin α1 had a higher expression in GM compared with WM and cortex, the other chains did not differ. Mutations in type IV collagen are known to cause fetal brain haemorrhage, hydrocephalus, porencephaly, cerebellar destruction and arterial aneurysms (Verbeek et al. 2012).  Prenatal lung ripening with glucocorticoids (GC) contributed to increased survival and less morbidity in preterm infants. The incidence of GMH-IVH is reduced by 50%. In a histopathological study of rabbits and human fetuses, prenatal GCs stabilized GM vasculature through suppressed angiogenesis, pruned neovasculature and enhanced pericyte coverage (Vinukonda et al. 2010).  In animal studies indomethacin inhibits prostaglandin synthesis and reduces blood flow. Ment et al. demonstrated that indomethacin in beagle pups led to increased deposition of collagen V and laminin, which increased stability of the basal lamina (Ment et al. 1992).  Not only are structures at the neurovascular unit fragile due to immaturity, some conditions (like acute and chronic hypoxia) disrupt the function of pericytes or astrocytes (Abbott et al. 2006, Sauders et al. 2018, Brown et al. 2019, Bell et al. 2020). germinal matrix fragility In a mouse model of limited GMH (not large IVH and no venous infarction) where GMH was created in anterior subventricular matrix on one side with injection of blood of the mouse itself, it was demonstrated that there is an increase of transient amplifying progenitors cells (Dawes et al. 2016). This increased cell production seems to exhaust the cell lines prematurely, because in the cortex above the lesion neurons do not increase in number. Oligodendroglial differentiation is also reduced in this model, best observed in the corpus callosum near the ventricle. This model shows how GMH may interfere with cell maturation in neuronal and glial lines without increasing cell death.  The fragility of vessels in GM is well known  but partly understood. Haemodynamic  factors seem to cause wall rupture in  small venules in many preterm infants  (Ghazi-Birry et al. 1997)).  Preterm brain haemorrhage occurs primarily in GM, but neither in cortex nor in white matter (El-Khoury et al. 2006). Matrix vascular density is increased compared to white matter and cerebral cortex (Ballabh et al. 2004). The vascular network of GM is complex, but regular anatomic schemes with arterioles, capillaries and veins are not present (Anstrom et al. 2004). GM vasculature drains along subependymal veins, in which medullary veins from the deep white matter coalesce between GM and caudate head (Bassan et al. 2009). At 23 weeks PMA thin-walled subependymal veins are well identified in GM; they mature with increasing GA. Pericytes are underrepresented in these vessels in human fetuses and preterm infants: both coverage and density were reduced in GM compared with WM and cortex (Braun et al. 2007). In the mouse, pericytes mature with delayed presence of desmin-positive pericyte coverage (cell stability) in GM (Nadeem et al. 2022). Contrary to the human the number of pericytes in mouse GM is not lower than in cortex. Vascular maturation is by increasing number of vessels parallel to matrix size, not by enlargement of vessels.   Blood-brain barrier (BBB) components include endothelial tight junctions, astrocyte end-feet coverage, basal lamina and capillary pericytes: all play a role in stabilisation of microvessels. Weakness of any of those components can predispose to GMH (Xu et al. 2008). Changes in BBB permeability correlate with the distribution of tight junction proteins (Ballabh et al. 2005), although the maturational role of tight junctions in development of GMH is controversial. In human GM at 24 weeks PMA tight junction proteins like ZO-1, claudin and occludin are present (thin discontinuous lines), but they are more abundant in cortical vessels (thick lines and nodes)(Anstrom et al. 2007). El-Khoury et al. compared perivascular coverage by astrocyte end-feet in GM with WM and cerebral cortex from 16 to 40 weeks PMA. They documented decreased expression of glial fibrillary acidic protein (GFAP) in end-feet along the vasculature of the GM (compared with WM and cortex) between 24-32 weeks. End-feet coverage plays a role in the fragility of GM vasculature.  The terminal vein (thalamostriate vein) drains into the internal cerebral vein together with the septal vein near the stria terminalis. GMH in a matrix pocket in this area can compress the terminal or septal vein or one of their adjacent branches.  This leads to medullary vein congestion, haemorrhagic diapedesis and finally venous infarction. On occasion one can observe with doppler that there may be an arterial ischaemic component to this infarction.  GMH arises near venules veins are cuffed by matrix collections in a scaffold germinal matrix and veins near the caudate head fragility issues In summary fragility of GM microvasculature is not likely due to lack of collagen, laminin or perlecan. Fibronectin is significantly lower in GM compared with WM and cortex and therefore might play a role. Tight junction protein levels in GM are comparable with WM and cortex levels, however these tight junctions are immature at 23 weeks of gestation and mature with increasing GA. Perivascular coverage by astrocyte end-feet is immature in GM. Prenatal use of GCs stabilizes GM vasculature. Prophylactic use of indomethacin might have a protective effect on the development of GMH.  germinal matrix fragility and disruption Anström et al. 2004 It is distension of venules that is the most likely cause of GMH. Notice the common occurrence of GMH in the roof of the temporal horn (Y) and especially around the caudothalamic groove (X). GMH is not always typically located in the caudothalamic groove, especially in ELBW infants. Nakamura et al. 1990 and 1991The location of GMH, depends on the nearby presence of collector veins. Notice the common occurrence of GMH in the roof of the temporal horn and especially around the caudothalamic groove. any bleeding 82 postmortems GMH site GMH risk factors, mainly haemodynamic in vital parameters it is sometimes possible to reconstruct the moment of haemorrhage detecting a rise in blood pressure and tachycardia Pryds et al. 1989, Debus et al. 1998, Meek et al. 1999, Adcock et al. 2003, Kluckow et al. 2004, Gopel et al. 2006, Dempsey et al. 2007, Miletin et al. 2008, Ramenghi et al. 2011, Harteman et al. 2012, Ballabh et al. 2014 The germinal matrix is a richly vascularized, transient layer at the surface of the ventricles, present in the fetal brain between 8 and 36 weeks PMA (Kinoshita et al. 2001). GM volume (GMV) reaches its maximum at 23-26 weeks PMA (Battin et al. 1998, Kinoshita et al. 2001, Habas et al. 2010). Scott et al. studied 48 MRI scans of 39 fetuses in utero between 20-31 weeks PMA. Using motion-corrected, automatic segmentation they showed that matrix volume peaks at 25 weeks, corroborated by histological studies (Scott et al. 2011, Del Bigio 2011). Reduction of this volume occurs site specific and continues until the subventricular zone regresses at 36 weeks.  germinal matrix evolution and involution GM is considered the ‘factory’ for production of brain cells: glutamatergic projection neurons, GABAergic interneurons and oligodendroglial as well as astroglial precursors in the latter part of pregnancy. After 15 weeks the subventricular zone becomes the predominant site of cell generation, forming ganglionic eminences along the lateral walls of the frontal horns of the lateral ventricles (Ulfig 2002, Del Bigio 2011). Neuroblasts from the eminences migrate tangentially to reach the cortical anlage along a scaffold of radial glial fibers. Neurons produced first migrate laterally (radially) and then change direction, entering tangential migration. Tangential migration is also seen in thalamic pulvinar as interneurons from the caudal GM migrate to the diencephalon during months 5-8 of gestation. As GM is a major source of oligodendrocytes, their production and differentiation can be impaired due to haemorrhage; this may contribute to white matter injury (Ulfig 2002). One can expect that subtle matrix lesions have an impact on late stages of formation of the cortical plate. Part of the subventricular zone persists, providing interneurons for the olfactory bulb and oligodendrocytes through adulthood (Corbin et al. 2008).  Pape and Wigglesworth (1979) described the development of arteries, capillaries and veins forming cerebral and cerebellar vascular beds. The matrix zone widens up to the 24th gestational week, its presence becomes prominent in the frontal horns and in the body of the lateral ventricle. After the 34th week pockets of matrix remain in the caudothalamic groove, the lateral wall of the occipital horn, the roof of the temporal and the tip of the frontal horn. Between 24 and 32 weeks PMA maturation is at a critical stage with ongoing events such as growth of axons, maximal growth of the subplate and entrance of thalamic afferents into the developing cortex. GMH prevention, management and prognosis Infants that suffer from grade 3 GMH-IVH have a significantly increased risk for neurodevelopmental disability, especially when complicated by post-hemorrhagic ventricular dilatation that needs surgical intervention. Cerebral palsy rates in infants with IVH grade 3 range between 7-63% (Brouwer et al. 2008, Adams-Chapman et al. 2008, Klebermass-Shrehof et al. 2012). Infants that suffer from mild low-grade (i.e. grade 1 or 2) GMH-IVH are clearly at much lower risk of developmental disabilities compared to infants with grade 3 GMH-IVH or IPL. Recent data suggest that this may not be entirely true (Patra et al. 2006, Klebermass-Shrehof et al. 2012). It has been shown that low-grade GMH-IVH is followed by microstructural impairment in the periventricular and subcortical white matter (Tortora et al. 2017). Size, number and location of these minor bleedings might be of importance in infants of the lowest gestational ages. In addition, germinal matrix injury even after an uncomplicated GMH-IVH results in a relevant loss of glial precursor cells, leading to impaired myelination and cortical development (Gressens et al. 1992, Vasileadis et al. 2004). GMH-IVH can also trigger inflammation in adjacent white matter through activated microglia, passage of red blood cells and red blood cell degradation: resulting tissue injury may be secondary to free radical release and the presence of free iron (Chen et al. 2011, Gram et al. 2013, Supramaniam et al. 2013, Ley et al. 2016).  The only single independent preventive factor that has been proven to decrease the risk for GMH-IVH and improve long term outcome is antenatal steroid treatment (Wapner 2013, Xu et al. 2008, Vinukonda et al. 2010). Postnatal indomethacin treatment has been shown to reduce the rate of severe IVH, particularly in male infants (Ment et al. 2004), but does not improve neurodevelopmental or sensory long-term outcome (Fowlie et al. 2010). Data on the preventive effect of delayed cord clamping are still conflicting, especially when the intrinsic risk of low gestational age is considered (Rabe et al. 2012, Tarnow-Mordi et al. 2017). GMH/IVH postmortem examples With CT, and later ultrasound, a classification was proposed in four grades (Papile et al. 1978, Pape and Wigglesworth 1979, Kuban and Teele 1984). Progression from GMH to IVH is still believed to follow mechanical rupture of bleeding under pressure, perhaps bursting through the weakest part of the ependymal lining at the stria terminalis, probably injured by some degree of hypoxia-ischaemia. Extension from limited to extensive IVH may relate to the cerebral perfusion pressure and deficient haemostasis. Progression to white matter or striatal infarction is due to compression of collector veins and is as such not a fourth grade but an association with any of the three genuine grades. Despite several ultrasound classifications subsequently published (Bowerman et al. 1984, Kuban and Teele 1984), the Papile classification, widely used for decades (Horbar et al. 2012) is now reduced to three grade: “grade 4” is now replaced by periventricular haemorrhagic venous infarction (PHI) (Volpe 1998, Paneth 1994). PHI can be associated to each grade of GMH-IVH. GMH/IVH grading grading 1.  limited to subependymal matrix (GMH) 2.  flooding of < 50% of the lateral ventricle and consequently without acute ventriculomegaly (limited IVH) 3. flooding of 50% or more of one or both lateral ventricles with acute distension by clot (extensive IVH) PHI  grades 1, 2 or 3 with periventricular haemorrhagic infarction in a more or less extensive area of the periventricular parenchyma limited GMH around an unstained (venous) matrix vessel In preterm brains, staining for endogenous alkaline phosphatase allows visual differentiation between afferent and efferent vessels. Germinal matrix haemorrhage in preterm neonates is primarily venous in origin (Ghazi-Birry et al. 1997). A haemorrhage tunnels along the perivenous space, compressing the vein and rupturing the tethered tributaries. Extravasation of blood from the arterial circulation appears to be much less common. Endothelium can be prone to injury following hypoxia and bleeding easily perpetuates due to enhanced fibrinolysis. alkaline phosphatase staining postmortem scans of twin with twin to twin transfusion at PMA 24w; acceptor with polycythaemia and congestion on top vaginal failed breech delivery followed by vacuum traction of second twin at 33w PMA, congested face and painful head without polycythaemia venous congestion preterm, lethal RDS: parietal flaring reflecting periventricular duskiness and venous distension at postmortem acute (unfibrinated) bleeding into the ventricle on day 2 and day 4 MR of a preterm at 28w GA; notice flaring on US and radial venous accentuation on T2 (dark stripes perpendicular to ventricle wall) Preceding venous infarction, veins may be distended by a large GMH or IVH, or by preceding head compression during delivery or high intra-thoracic pressures for instance. There is no definite diagnostic method for congestion. Congested medullary veins, descending from subcortex to lateral or medial subependymal collector veins near the terminal vein, fanning out from the ventricle border, contribute to periventricular flaring by the increased amount of cellular scatterers (Takashima and Tanaka 1978). For this reason it is difficult to evaluate white matter changes near GMH/IVH (Ramenghi et al. 2002). Congestion is expected to releave with time. Distended medullary veins should form a hyperechoic fan near the ventricle; heterogeneous echobright focal change within “flaring" may indicate haemorrhagic diapedesis, frank haemorrhage or infarction. There is a spared subcortical rim of tissue drained towards the pial coverings. Ischaemia (restricted diffusion on DW MRI) with a linear pattern perpendicular to the ventricle lumen, can on occasion be seen along these medullary veins. The term post-haemorrhagic ventricular dilatation (PHVD) refers to dilatation of the cerebral ventricles subsequent to GMH-IVH. Approximately 25% of infants with GMH-IVH develop progressive PHVD (Murphy et al. 2002). The risk for PHVD is higher following severe GMH-IVH (i.e. grade III GMH-IVH or PHI) (Brouwer et al. 2015). The vast majority of progressive PHVD (80%) follow IVH III, often in combination with a PHI. While in the majority PHVD will eventually resolve (approximately 40% spontaneously and another 15% after non-surgical treatment), around 35% of infants with progressive PHVD require surgical treatment, while 10% die (Murphy et al. 2002). Despite decades of research, treatment of PHVD remains a challenge (Brouwer et al. 2014, Bravo et al. 2024). Several options were investigated: lumbar or ventricular tapping, CSF drainage and fibrinolytic treatment, surgical insertion of an external drain, a subcutaneous reservoir, and permanent ventriculo-peritoneal shunt. The key problem is to balance between the adverse effect of PHVD on the immature brain and the risk for adverse effects of interventions (e.g. CSF infection related to CSF tapping, secondary bleeding after fibrinolytic treatment, decompression bleeding) (Robinson et al. 2012, Bravo et al. 2024).  PHVD is strongly associated with neurodevelopmental impairment, particularly in infants with persistent PHVD that requires surgical intervention and if PHVD is combined with PHI (Adams-Chapman et al. 2008). Recent studies suggest a better outcome than reported earlier (Brouwer et al. 2008 and 2012). This might reflect a different lesion mix and/ora heterogeneity of management strategies among centres. A recent multicenter study showed that early treatment of PHVD, based on ventricular measurements, is associated with favourable neurodevelopmental outcomes, even when a permanent shunt is eventually needed (Leijser et al. 2018).  PHVD is due to imbalance between production and resorption of CSF. It usually develops a few days to a few weeks after IVH, although exceptionally rare cases developing after term-equivalent age have been reported (de Vries et al. 2000, Whitelaw 2001). Despite PHVD is more frequent after grade III GMH-IVH and PHI, it may complicate each grade (Murphy et al. 2002). For this reason, serial ultrasound scans are warranted following GMH-IVH, at least until term-equivalent age. Obstruction to CSF circulation at various levels by clots or by fibrin debris contributes to the problem. The patient can develop various types of PHVD according to the location of such obstruction(s): - unilateral PHVD following unilateral obstruction of Monro foramen - supratentorial (triventricular) PHVD following aqueduct obstruction - complete internal (tetraventricular) hydrocephalus following obstruction of the fourth ventricle outlets (Luschka and Magendi foramina) - complete internal and external hydrocephalus (also referred to as communicating hydrocephalus) following impairment of CSF reasorption in the pericerebral arachnoid spaces - in some cases, the fourth ventricle is isolated from CSF circulation by concomitant obstruction of the aqueduct and of the fourth ventricle outlets (Rademaker et al. 1995, Whitelaw 2001, Murphy et al. 2002). post-haemorrhagic ventricular dilatation (PHVD)  Preterm infants are often unstable during the first days of life, when GMH-IVH typically presents. CUS is non-invasive and suitable for repeated examinations, allowing prompt diagnosis of GMH-IVH as well as assessment of its evolution (Ramenghi et al. 2005). In the critical phase, CUS should be as “quick and gentle” as possible, in order to minimize stress in these fragile neonates. As the incidence of GMH-IVH is closely related to gestational age at birth (Sannia et al. 2015), it seems reasonable to recommend the following schedule: in preterm infants with a gestational age below 28 weeks or 1000 grams, serial CUS should be performed on day 1, 3, 7, 14, 21, 28, and then every other week until term-equivalent age. In stable preterm infants with a gestational age above 28 weeks, the frequency of serial CUS can be limited to day 1, 3, 7, 14, 28, at six weeks and at term-equivalent age. More frequent examinations are advisable in case of clinically suspected bleeding or because of subtle or unclear CUS findings) (van Wezel-Meijler 2007). CUS examinations beyond the first week of life allow the detection of PHVD as well as of uncommon cases of late-onset GMH-IVH.  Evolution. Ultrasonographic changes over time should be kept in mind in order to consider the antenatal origin of IVH when subacute characteristics of the clot are observed soon after birth, or to suspect an IVH already in its earliest, hyperacute phase. As previously stated, the most typical clue for a GMH-IVH is a subependymal and/or intraventricular hyperechoic clot detected during the first postnatal days. Hyperechogenicity is due to fibrin formation at the end of the clotting cascade and is the main feature of the clot between 4-6 hours and 3 days after the bleeding (Dewbury et al. 1983). In the earliest phase, fresh IVH may remain hypo- or isoechoic, and motion of particulate CSF can sometimes be visible within the ventricles. In the subacute phase, after an initial retraction, the clot is characterized by progressive hypoechoic changes in the central portion and by hyperechoic margins. Intraventricular fibrin strands surrounding the clot may be observed. In some, intraventricular clot fragments can be detected by CUS for months (Govaert and de Vries 2010).  Besides cerebellar haemorrhage, an uncommon type of bleeding that can be found associated with GMH-IVH in preterm infants is septal haemorrhage. The classical sonographic finding is the presence of a clot in the cavum septi pellucidi and/or in the cavum Vergae. Septal haemorrhage may derive from septal veins or from extension of IVH following the rupture of one septal leaflet (Koumanidou et al. 2002).  Plexus haemorrhage has been described associated to GMH-IVH in neuropathological studies of VLBW infants (Armstong et al. 1987, Paneth 1994). However, identifying a plexus hemorrhage and to ddistinguish it from GMH-IVH is challenging for the sonographer.  When bleeding is limited to germinal matrix (GMH), the typical finding is a subependymal hyperechoic globular focus detected during the first week of life, that usually remains visible for a few weeks. It may bulge into the lumen. As in some cases it is difficult to distinguish a small GMH from the adjacent hyperechoic choroid plexus, both coronal and parasagittal scans should be carefully examined before a diagnosis of GMH is retained (Bowerman et al. 1984, Shackelford and Volpe 1985, Hope et al. 1988). The most anterior portion of the plexus is thin and ends at the level of the caudo-thalamic groove; plexus thickens posteriorly, is not visible in the frontal and occipital horns of the lateral ventricle and produces a near symmetrical picture in coronal planes (Govaert and de Vries 2010). Asymmetric hyperechoic thickening at the caudo-thalamic groove (the most common location for GMH) on coronal planes occurring in the first postnatal days strongly suggests unilateral GMH. Of course, GMH may also occur bilaterally, rarely symmetrical. Conversely, an echogenicity developing at the groove in the late neonatal period should suggest a hyperechoic germinolysis rather than a late GMH (Horsch et al. 2010, Raets et al. 2015). Post-mortem studies confirmed that the majority of GMHs develop in the caudo-thalamic region, although pathologic evidence of subependymal bleeding may be found also in the occipital and temporal horns: these regions should be carefully examined during CUS. Accuracy of CUS for minor forms of GMH-IVH is suboptimal when compared to the MR-SWI sequence, which is considered the most sensitive technique for detection of small haemorrhages (Parodi et al. 2015).  In some instances, the ependymal layer surrounding germinal matrix ruptures, allowing extension from matrix into the ventricle lumen (IVH). IVH can be limited (filling less than 50% of the lateral ventricle on parasagittal view) or extensive (filling 50% or more). The extension from GMH to stria terminalis may isolate parts of the caudate head, creating the impression of cavitation in early scans. IVH is usually suggested by hyperechoic clot located anterior to the foramina of Monro, above the caudo-thalamic groove or in the occipital horn. Insonation through the posterior or even mastoid fontanel may allow better visualization of clot (Bowerman et al. 1984). However, identification of a minimal amount of intraventricular blood (i.e. the distinction between a “pure” subependymal GMH and a very limited IVH) remains challenging in absence of an obvious intraventricular clot. In this case, hyperechoic ependyma and infratentorial clot are indirect signs that corroborate a diagnosis of IVH (Rypens et al. 1994): hyperechoic ependymal changes occur from 2 to 4 weeks after an IVH, while clots of blood from supratentorial origin can be detected in the fourth ventricle and in the cisterna magna by insonating through the mastoid fontanel.  A large clot filling the ventricle and causing acute dilatation of the involved lateral ventricle(s) is typical of extensive IVH. Acute ventricular dilatation occurs by the mass effect of clot; this phenomenon should be distinguished from post-haemorrhagic ventricular dilatation, which takes place after few days or weeks and is due to an imbalance between CSF production and reabsorption, complicated by clot crowding in the posterior fossa around the cerebellum.  GMH/IVH in cranial ultrasound Medullary veins from just below the subcortex drain into deep veins, gradually coalescing into larger trunks (Okudera et al. 1999). This high drainage with a peculiar organisation of confluence explains the feathered appearance of the outer (subcortical) contour of a medullary venous infarct. It also explains the triangular shape as veins fan out from the ependymal collectors near the GMH. medullary veins PHI (periventricular haemorrhagic infarction) complicates GMH-IVH in approximately 15% of cases (Golden et al. 1997, Larroque et al. 2003). GMH-IVH of all grades can be complicated by PHI, but the higher the grade the more likely PHI is to occur (Guzetta et al. 1986). PHI is caused by venous obstruction induced by GMH-IVH. Venous congestion leads to ischaemia and to secondary haemorrhagic infarction. High intraventricular pressure dilating the ventricles due to a large IVH may additionally affect flow through the subependymal veins, increasing infarct size (Volpe 1998). Cerebral palsy and severe cognitive impairment are common in infants who suffered from PHI (Brouwer et al. 2008, Adams-Chapman et al. 2008, Klebermass-Shrehof et al. 2012)). Prognosis is highly dependent on localization and extent of the lesion (Bassan et al. 2006 and 2007, Dudink et al. 2008, Maitre et al. 2009). Classifying PHI into venous subtypes helps to predict outcome and counsel parents in this difficult situation (Dudink et al. 2008). Mortality in infants with extensive PHI is high, especially when it occurs bilaterally. In many countries, redirection of care and end of life decisions are considered in infants with bilateral PHI. Although robust data on this are lacking, it is likely that redirection of care contributes significantly to the reported mortality rates (Davis et al. 2014, Sheehan et al. 2017). PHI, also referred to as parenchymal haemorrhagic infarction, or periventricular venous infarction, or intraparenchymal lesion, can complicate each grade of GMH-IVH and seems to occur a few hours up to a few days after the initial GMH (Perlman et al. 1993). Post-mortem and doppler studies strongly suggest that this lesion is due to venous infarction following venous obstruction and congestion (Takashima et al. 1986, Gould et al. 1987, Nakamura et al. 1990 and 1991, Paneth et al. 1994, Taylor 1995, Ghazi-Birry et al. 1997, Volpe 1998). It has also been suggested that parenchymal ischaemia secondary to venous obstruction contributes to injury (Toft et al. 1997). The typical ultrasonographic appearance of PHI is a triangular, “fan-shaped” hyperechoic lesion in periventricular white matter, ipsilateral to the GMH-IVH (Guzzetta et al. 1986). In the earliest phase, the lesion appears separated from the ventricular wall; it may subsequently grow, touch the ventricular wall and eventually merge into a single, large hyperechoic change together with the initial GMH-IVH. The parenchymal hyperechoic area tends to decrease after few days: this is believed to reflect the regression of venous congestion around it, leading to overestimation of the real extent (Govaert and de Vries 2010).  When PHI complicates GMH (or a very limited IVH), it often remains separated from the initial GMH, appearing as a small hyperechoic lesion in the ipsilateral white matter. Multiple minute PHIs along the course of the medullary veins can also be observed. We speculate that these minor PHIs may result from a partial venous obstruction due to compression of a subependymal vein. The risk of developing PHI following GMH might also be related to the location of the GMH itself, especially in subjects with a peculiar venous anatomy prone to congestion.  Venous infarction in relation to venous anatomy is descrived in detail with a separate white matter item. parenchymal haemorrhagic infarction associated with GMH/IVH PHI usually evolves into a cavity within periventricular white matter. As most PHIs develop adjacent to the ventricular wall, porencephaly resulting from the cavity as it merges with the ventricle is a common observation after one or two months (Grant et al. 1982, Donn and Bowerman 1982, Fleischer et al. 1983). Regardless of the evolution into porencephaly, a cavitation resulting from PHI is usually single, asymmetric and persistent. Conversely, cysts of periventricular leukomalacia typically appear with symmetrical, mainly posterior distribution and tend to disappear within few weeks, insomuch that they are often undetectable at term-equivalent age (Pierrat et al. 2001). Size and location of PHI depend on which vein is involved in the process of venous obstruction. In some cases, more veins are involved, leading to an extensive unilateral PHI or to a much rarer bilateral PHI (Bassan et al. 2006, Dudink et al. 2008). The extensive IPL is extremely echoic, shows irregular, feathered borders with the cortex and allows no separation between density and ventricular clot (Perlman et al. 1993, Rademaker et al. 1994). Because a diagnosis of PHI carries important prognostic implications (Maitre et al. 2009, Sheehan et al. 2017), classification should be clinical routine. Dudink et al 2008 classified PHI based on venous anatomy and correlated this with outcome. Of course, advanced MRI techniques like DTI and SWI add useful information for prediction of outcome (Roze et al. 2015). Access to MRI is often limited by obvious logistic obstacles in the acute or early subacute phase of PHI. Recognizing the venous subtype of PHI with CUS, rather than labelling the lesion as unspecified PHI, can help the clinician to predict neurological outcome, allowing the start of a targeted rehabilitation program at an early stage, and may enrich the quality of family counselling.  GMH/IVH postmortem example GMH and IVH (courtesy S Brock, UZ Brussel) H&E staining at 24w PMA (courtesy JS Wigglesworth Hammersmith Hospital) To understand the images involved in venous infarction a schematic insight into deep vein anatomy is necessary. A venous infarct occurs from a few hours up to a few days after the initial GMH, and location and size vary. A venous mechanism was first postulated decades ago; later conflicting views about parenchymal extension and parenchymal infarction have been reviewed in detail by Paneth et al. (1994). Postmortem studies by Gould et al. (1986), Takashima et al. (1986), Nakamura et al. 1990 and 1991, and Ghazi-Birry et al. 1997 strongly suggest the parenchymal lesion is venous infarction. GMH and (large) veins 12 inferior striate vein 13 anterior cerebral vein 14 deep middle cerebral vein (insular vein) 15 inferior ventricle vein 16 inferior choroidal vein 17 lateral mesencephalic vein 18 lateral atrial vein 19 precentral cerebellar vein 20 superior vermis vein 21 inferior sagittal sinus 22 septal vein 1 sinus rectus (straight sinus) 2 great cerebral vein of Galen 3 internal cerebral vein 4 terminal (thalamo-striate) vein 5 longitudinal caudate vein 6 medullary veins to caudate collector veins 7 superior choroidal vein 8 direct lateral vein (surface thalamic vein) 9 superior thalamic vein 10 medial atrial vein 11 basal vein of Rosenthal deep vein variation The (variable) shape and size of veins, still very developmental in third trimester, plays a role in the occurrence and evolution of GMH and IVH. Veins near matrix areas are at risk of compression by expanding GMHs. The fragile sites are mainly near the transition of internal cerebral to terminal vein, and near the inferior ventricle vein. There is an ongoing interest in variations in anatomy and in flow pattern that may predispose to GMH and its sequelae (Stein and Rosenbaum 1974, Takashima et al. 1986, Gould et al. 1987, Wang et al. 2010, Taoka et al. 2017, Tortora et al. 2018, Kent et al. 2023, Camfferman et al. 2026, Steinsmo Odegard et al. 2026). A comprehensive example of deep vein classification for further study is below. One example of such variation is the U-turn of the trasniation from terminal vein to internal cerebral vein (Larroche 1977), in recent papers studied for the position and degree of acuity of the angle.  cuffs around veins Subependymal vein precursors grow in diameter from 23 weeks to term. The wall of the veins, at early stages with endothelial cells only, does not thicken until after week 36 (added second layer of cells). The largest veins develop at three specific regions: caudothalamic groove, caudate to matrix border and superolateral ventricle angle.  ——> in all viable premature neonates, the subependymal veins are present and appear vulnerable to rupture The association of cuffs of matrix cells above the caudate head, to veins crossing through matrix (Anstrom et al. 2005) is an explanation for the finding that most GMHs follow distension of veins, and are not due to not primary thrombosis. Secondly, the matrix cells form a cuff around the vein, the cuff itself is bordered by a glial scaffold and from this perimeter processes extend to the vessel itself. This provides corridors for cell migration. This migration guided by glial processes resembles chain migration, e.g. in the corpus gangliothalamicum. Using staining with alkaline phosphatase (arteries and capillaries, not veins) and collagen A4 (all vessels) Anström et al. challenge the idea that fragility is the main reason for preterm GMH (Anstrom et al. 2005). There are three vascular areas in matrix. A subependymal network has predominantly veins organised in a plexus of around 50 µm thick. A central area is vessel-poor but has small arteries, venules and capillaries, some aligned perpendicular to the ependymal line; in this area clusters of matrix cells form a package lined by vessels and glial (GFAP-positive) fibers, whereas other areas lack this clustering and have vessels oriented in all directions. Finally, near the caudate head both veins and arteries form a dense cluster of vessels. There is no evidence of interarterial border zones. Capillaries in matrix do not differ in maturity from those in cortex, but many small veins with somewhat larger caliber are the most likely site of vessel disruption in preterm GMH, not the capillaries.  clot in cavum Vergae hyperechoic ependyma large v4 clot cisternal change overview a onset after day 2 with congestion on calcar avis IVH in ultrasound overview b typical limited IVH large clots extensive IVH subventricular echogenicity due to germinolysis: bilateral often symmetrical, early or often late onset, unexplained by haemodynamic events, evolving in weeks to months; no sign of haemorrhage on MRI GMH versus hyperechoic germinolysis GMH: unilateral or asymmetrical, evolving in days to weeks, haemodynamic context, signs of IVH or infarction; dark on T2 or SSWI  post-haemorrhagic ventricular dilatation (PHVD): ultrasound methods of follow-up  Some patients show transient PHVD with a stable phase followed by regression of dilatation within days or a few weeks (Levene and Starte 1981). Progression of PHVD can be easily detected by measurement of the lateral ventricles. Percentile graphs for these were published decades ago and recently reviewed (Levene 1981, Davies et al. 2000, Brouwer et al. 2012). Ventricular Index (VI) and Anterior Horn Width (AHW), both obtained in a coronal plane passing through the foramina of Monro, are commonly used. Absence of significant widening of the frontal horns may lead to underestimation of PHVD severity, as neonates tend toward colpocephaly (Brann et al. 1991). Thalamo-Occipital Distance (TOD) is measured in the parasagittal plane and reflects dilatation of the trigone and the occipital horn. Reproducibility of these ventricular measurements (VI, AHW and TOD) was at least good in two studies assessing both intra- and inter-observer reliability (Davies et al. 2000, Brouwer et al. 2012). VI and AHW are used in European NICUs to define the threshold for treatment: although no consensus exists, the majority initiate treatment once the ventricular width crosses the 97th percentile + 4 mm line on Levene’s graph (Brouwer et al. 2012, Bravo et al. 2024).  Common in severe PHVD are a rounded upper border of the frontal horns in coronal planes (“ballooning”) (Brouwer et al. 2008) and a rounded profile of the third ventricle in the midsagittal plane, due to the markedly dilated infundibular and supraoptic recess. Dilatation of the fourth ventricle is identified in the midsagittal plane in case of tetraventricular or communicating hydrocephalus. Routine use of additional acoustic windows provide information to understand the type of PHVD: insonation through the suture between the temporal and the parietal bone, above the ear, can show a markedly dilated aqueduct in case of tetraventricular or communicating hydrocephalus, as well as an obstructed aqueduct in case of triventricular hydrocephalus. By gently tilting and rotating the probe in a pseudo-axial plane, the sonographer should aim to obtain the third ventricle and the fourth ventricle connected by the aqueduct depicted in the same image. GMH IVH extensive day 13 diapedesis along medial subependymal veins GMH/IVH grading: typical ultrasound scans and MRI day 6 ventricular dilatation 31w GA, T2 MRI Mac OS X  2°âATTRâ¼&¼com.apple.TextEncodingËcom.apple.quarantineutf-8;134217984q/0082;6a1f1ef7;Hype4;