ASPHYXIA CORTEX - keywords
asphyxia cortex
Adamsons K, Mueller-Heubach E, Myers RE: Production of fetal asphyxia in the rhesus monkey by administration of catecholamines to the mother. Am J Obstet Gynecol 109:248-262, 1971
Alderliesten T, Nikkels PG, Benders MJ, de Vries LS, Groenendaal F. Antemortem cranial MRI compared with postmortem histopathologic examination of the brain in term infants with neonatal encephalopathy following perinatal asphyxia. Arch Dis Child Fetal Neonatal Ed 2013; 98(4):F304-309.
Alderliesten T, Wagenaar N, van der Aa NE, Lequin MH, Benders MJNL, van Haastert IC, Groenendaal F. MRI Changes in the Thalamus and Basal Ganglia of Full-Term Neonates with Perinatal Asphyxia. Neonatology 2018; 114(3):253-260.
Ahdab-Barmada M, Moossy J. The neuropathology of kernicterus in the premature neonate: diagnostic problems. J Neuropathol Exp Neurol 1984; 43(1):45-56.
Alderliesten T, Parmentier CEJ, Benders MJNL, de Vries LS, Vijlbrief DC, Dudink J, Tataranno ML, Lemmers PMA, Groenendaal F, van Bel F. Cerebral Oxygenation Pattern during Therapeutic Hypothermia after Perinatal Asphyxia: A Single Center Cohort Study. Neonatology. 2025;122(6):741-750. 12668717.
Annink KV, de Vries LS, Groenendaal F, Vijlbrief DC, Weeke LC, Roehr CC, Lequin M, Reiss I, Govaert P, Benders MJNL, Dudink J. The development and validation of a cerebral ultrasound scoring system for infants with hypoxic-ischaemic encephalopathy. Pediatr Res. 2020; 87(Suppl 1):59-66.
Arend I, Rafal R and Ward R. Spatial and temporal deficits are regionally dissociable in patients with pulvinar lesions. Brain 2008; 131: 2140–2152.
Aravamuthan BR, Waugh JL. Localization of basal ganglia and thalamic damage in dyskinetic cerebral palsy. Pediatr Neurol 2016; 54:11–21.
Babcock, D., Ball, W. (1983) ‘Postasphyxial encephalopathy in full-term infants : ultrasound diagnosis.’, Radiology, 148, 417-423.
Baker SN. The primate reticulospinal tract, hand function and functional recovery. J Physiol 2011; 589: 5603–5612.
Banker, B.Q., Larroche, J-Cl. (1962) Archives of Neurology, 7, 386-410.
Barkovich AJ, Westmark K, Partridge C, Sola A, Ferriero DM. Perinatal asphyxia: MR findings in the first 10 days. Am J Neuroradiol. 1995 Mar;16(3):427-38.
Barkovich AJ, Miller SP, Bartha A, Newton N, Hamrick SE, Mukherjee P, Glenn OA, Xu D, Partridge JC, Ferriero DM, Vigneron DB. MR imaging, MR spectroscopy, and diffusion tensor imaging of sequential studies in neonates with encephalopathy. AJNR Am J Neuroradiol 2006; 27(3):533-547.
Bednarek N, Mathur A, Inder T, Wilkinson J, Neil J, Shimony J. Impact of therapeutic hypothermia on MRI diffusion changes in neonatal encephalopathy. Neurology. 2012 May 1;78(18):1420-7.
Bonifacio SL, Glass HC, Vanderpluym J, Agrawal AT, Xu D, Barkovich AJ, Ferriero DM. Perinatal events and early magnetic resonance imaging in therapeutic hypothermia. J Pediatr 2011; 158(3):360-365.
Brann AW Jr, Myers RE. Central nervous system findings in the newborn monkey following severe in utero partial asphyxia. Neurology 1975; 25:327–338.
Brambrink AM, Martin LJ, Hanley DF, et al. Effects of the AMPA receptor antagonist NBQX on outcome of newborn pigs after asphyxic cardiac arrest. J Cereb Blood Flow Metab 1999; 19: 927–938.
Brambrink AM, Ichord RN, Martin LJ, et al. Poor outcome after hypoxia-ischemia in newborns is associated with physiological abnormalities during early recovery. Possible relevance to secondary brain injury after head trauma in infants. Exp Toxicol Pathol 1999; 51: 151–162.
Cahill-Rowley K and Rose J. Etiology of impaired selective motor control: emerging evidence and its implications for research and treatment in cerebral palsy. Dev Med Child Neurol 2014; 56: 522–528.
Chugani HT, Phelps ME. Imaging human brain development with positron emission tomography. J Nucl Med. 1991 Jan;32(1):23-6.
Chugani HT, Phelps ME. Maturational changes in cerebral function in infants determined by 18FDG positron emission tomography. Science. 1986 Feb21;231(4740):840-3.
Chugani HT, Phelps ME, Mazziotta JC. Positron emission tomography study of human brain functional development. Ann Neurol. 1987 Oct;22(4):487-97.
Clancy RR, Sladky JT and Rorke LB. Hypoxic-ischemic spinal cord injury following perinatal asphyxia. Ann Neurol 1989; 25: 185–189.
Gilles FH and Murphy SF. Perinatal telencephalic leucoencephalopathy. J Neurol Neurosurg Psychiatry 1969; 32: 404–413.
Connolly, B., Kelehan, P., O'Brien, N., Gorman, W., Murphy, J.F., King, M., Donoghue, V. (1994) ‘The echogenic thalamus in hypoxic ischaemic encephalopathy.’, Pediatric Radiology, 24, 268-271.
Cowan, F.M., Pennock, J.M., Hanrahan, J.D., Manji, K.P., Edwards, A.D. (1994) ‘Early detection of cerebral infarction and hypoxic ischemic encephalopathy in neonates using diffusion-weighted magnetic resonance imaging.’, Neuropediatrics, 25, 172-175.
Couture, A. (1994) ‘Les lésions cérébrales anoxo-ischémiques.’, in Couture, A., Veyrac, C., Baud, C. (Eds) Echographie cérébrale du foetus au nouveau-né, Montpellier : Sauramps Médical, pp 183-248.
Craner SL and Ray RH. Somatosensory cortex of the neonatal pig: I. Topographic organization of the primary somatosensory cortex (SI). J Comp Neurol 1991; 306: 24–38.
de Haan HH, Gunn AJ, Williams CE, et al. Brief repeated umbilical cord occlusions cause sustained cytotoxic cerebral edema and focal infarcts in near-term fetal lambs. Pediatr Res 1997; 41: 96–104.
de Haan HH, Gunn AJ, Williams CE, et al. Magnesium sulfate therapy during asphyxia in near-term fetal lambs does not compromise the fetus but does not reduce cerebral injury. Am J Obstet Gynecol 1997; 176: 18–27.
de Vries LS and Groenendaal F. Patterns of neonatal hypoxic-ischaemic brain injury. Neuroradiology 2010; 52: 555–66.
De Wispelaere LA, Ouwehand S, Olsthoorn M, Govaert P, Smit LS, de Jonge RC, Lequin MH, Reiss IK, Dudink J. Electroencephalography and brain magnetic resonance imaging in asphyxia comparing cooled and non-cooled infants. Eur J Paediatr Neurol. 2019 Jan;23(1):181-190.
Edwards AD, Yue X, Cox P, Hope PL, Azzopardi DV, Squier MV, Mehmet H (1997) Apoptosis in the brains of infants suffering intrauterine cerebral injury. Pediatr Res 42(5):684-9.
Eken, P., Jansen, G.H., Groenendaal, F., Rademaker, K., de Vries, L.S. (1994) ‘Intracranial lesions in the full term infant with hypoxic- ischaemic encefalopathy : ultrasound and autopsy correlation.’, Neuropediatrics, 25, 301-307.
Ellis WG, Goetzman BW, Lindenberg JA (1988) Neuropathologic documentation of prenatal brain damage. Am J Dis Child 142:858-866.
Fahey JO (2014) The Recognition and Management of Intrapartum Fetal Heart Rate Emergencies: Beyond Definitions and Classification. Journal of Midwifery & Women’s Health.
Faro MD, Windle WF. Transneuronal degeneration in brains of monkeys asphyxiated at birth. Exp Neurol. 1969 May;24(1):38-53.
Ferrari F, Todeschini A, Guidotti I, Martinez-Biarge M, Roversi MF, Berardi A, Ranzi A, Cowan FM, Rutherford MA. General movements in full-term infants with perinatal asphyxia are related to Basal Ganglia and thalamic lesions. J Pediatr. 2011 Jun;158(6):904-11.
Friede RL (1989) Developmental neuropathology. Berlin/Heidelberg : Springer-Verlag.
Gancia P, Pomero G. Brain cooling therapy. Minerva Pediatr. 2010 Jun;62(3 Suppl 1):173-5. PMID: 21089736.
Gleason CA, Hamm C and Jones MD Jr. Cerebral blood flow, oxygenation, and carbohydrate metabolism in immature fetal sheep in utero. Am J Physiol Regulatory Integrative Comp Physiol 1989; 256: R1264–R1268.
Gleason CA, Hamm C and Jones MD Jr. Effect of acute hypoxemia on brain blood flow and oxygen metabolism in immature fetal sheep. Am J Physiol Heart Circ Physiol 1990; 258: H1064–H1069.
Golden WC, Brambrink AM, Traystman RJ, et al. Failure to sustain recovery of Na,K-ATPase function is a possible mechanism for striatal neurodegeneration in hypoxic-ischemic newborn piglets. Brain Res Mol Brain Res 2001; 88: 94–102.
Govaert P, Zingman A, Jung YH, Dudink J, Swarte R, Zecic A, Meersschaut V, van Engelen S, Lequin M. Network injury to pulvinar with neonatal arterial ischemic stroke. Neuroimage. 2008 Feb 15;39(4):1850-7.
Graham DI (1992) Hypoxia and vascular disorders., in Adams, J.H., Duchen, L.W. (Eds) Greenfield’s Neuropathology, fifth edition, London : Edward Arnold, chapter 4, pp 153-268.
Gunn AJ, Parer JT, Mallard EC, et al. Cerebral histologic and electrocorticographic changes after asphyxia in fetal sheep. Pediatr Res 1992; 31: 486–491.
Gunn AJ, Gunn TR, de Haan HH, Williams CE, Gluckman PD. Dramatic neuronal rescue with prolonged selective head cooling after ischemia in fetal lambs. J Clin Invest. 1997 Jan 15;99(2):248-56.
Gunn AJ, Maxwell L, De Haan HH, et al. Delayed hypotension and subendocardial injury after repeated umbilical cord occlusion in near-term fetal lambs. Am J Obstet Gynecol 2000; 183: 1564–1572.
Hagberg H (2004) Mitochondrial impairment in the developing brain after hypoxia-ischemia. Journal of Bioenergy and Biomembranes 36(4):369-73.
Hankins GD, Speer M (2003) Defining the pathogenesis and pathophysiology of neonatal encephalopathy and cerebral palsy. Obstetr Gynecol 102: 628-636.
Hayashi M, Satoh J, Sakamoto K, Morimatsu Y. Clinical and neuropathological findings in severe athetoid cerebral palsy : a comparative study of globo-Luysian and thalamo-putaminal groups. Brain Development 1991; 13:47-51.
Huang, C.-C., Ho, M-Y., Shen, E-Y. (1987) ‘Sonographic changes in a parasagittal cerebral lesion in an asphyxiated newborn.’, Journal of Clinical Ultrasound, 15, 68-70.
Imai K, de Vries LS, Helou SM, Koehler RC, Gleason CA, et al. Cerebrovascular autoregulation during fetal development in sheep. Am J Physiol Heart Circ Physiol 1994; 266: H1069–H1074.
Imai K, de Vries LS, Alderliesten T, Wagenaar N, van der Aa NE, Lequin MH, Benders MJNL, van Haastert IC, Groenendaal F. MRI Changes in the Thalamus and Basal Ganglia of Full-Term Neonates with Perinatal Asphyxia. Neonatology. 2018;114(3):253-260.
Johnston MV, Hoon AH (2000) Possible mechanisms in infants for selective basal ganglia damage from asphyxia, kernicterus, or mitochondrial encephalopathies. J Child Neurol 15:588-591.
Johnston MV. Selective vulnerability in the neonatal brain. Ann Neurol 1998; 44: 155–156.
Johnston MV (2005) Excitotoxicity in perinatal brain injury. Brain Pathology 15(3):234-40.
Jones EG, Coulter JD, Burton H, et al. Cells of origin and terminal distribution of corticostriatal fibers arising in the sensory-motor cortex of monkeys. J Comp Neurol 1977; 173: 53–80.
Jones MD Jr., Sheldon RE, Peeters LL, et al. Regulation of cerebral blood flow in the ovine fetus. Am J Physiol Heart Circ Physiol 1978; 235: H162–H166.
Jones MD Jr., Traystman RJ, Simmons MA, et al. Effects of changes in arterial O2 content on cerebral blood flow in the lamb. Am J Physiol Heart Circ Physiol 1981; 240: H209–H215.
Jones MD Jr., Rosenberg AA, Simmons MA, et al. Oxygen delivery to the brain before and after birth. Science 1982; 216: 324–325.
Jouvet P, Cowan FM, Cox P, Lazda E, Rutherford MA, Wigglesworth J, Mehmet H, Edwards AD. Reproducibility and accuracy of MR imaging of the brain after severe birth asphyxia. Am J Neuroradiol. 1999 Aug;20(7):1343-8.
Juul SE, et al. Prenatal cord clamping in newborn macaca nemestrina: a model of perinatal asphyxia. Dev Neurosci 2007;29:311–20.
Koehler RC, Yang Z-J, Lee JK, Martin LJ (2018) Perinatal hypoxic-ischemic brain injury in large animal models: Relevance to human neonatal encephalopathy. Journal of Cerebral Blood Flow & Metabolism 38(12) 2092–2111.
Kostandy BB. The role of glutamate in neuronal ischemic injury: the role of spark in fire. Neurol Sci. 2012 Apr;33(2):223-37.
Kreusser, K.L., Schmidt, R.E., Shackelford, G.D., Volpe, J.J. (1984) ‘Value of ultrasound for identification of acute hemorrhagic necrosis of thalamus and basal ganglia in an asphyxiated term infant.’, Annals of Neurology, 16, 361-363.
Krägeloh-Mann I, Helber A, Mader I, Staudt M, Wolff M, Groenendaal F, DeVries L. Bilateral lesions of thalamus and basal ganglia: origin and outcome. Dev Med Child Neurol 2002; 44(7):477-484.
Kuenzle, C., Baenziger, O., Martin, E., Thun-Hohenstein, L., Steinlin, M., Good, M., Fanconi, S., Boltshauser, E., Largo, R.H. (1994) ‘Prognostic value of early MR imaging in term infants with severe perinatal asphyxia.’, Neuropediatrics, 25, 191-200.
Langeslag JF, Groenendaal F, Roosendaal SD, de Vries LS, Onland W, Leeflang MMG, Groot PFC, van Kaam AH, de Haan TR; PharmaCool Study Group. Outcome Prediction and Inter-Rater Comparison of Four Brain Magnetic Resonance Imaging Scoring Systems of Infants with Perinatal Asphyxia and Therapeutic Hypothermia.Neonatology. 2022;119(3):311-319.
Larroche J-C (1968) Nécrose cérébrale massive chez le nouveau-né. Biol Neon 13:340-360.
Larroche JC and DeVries L. Fetal and neonatal brain damage. In: Gilbert-Barness E (ed.) Potter’s pathology of the fetus and infant. Vol. 2, St. Louis, MO: MosbyYear Book, Inc., 1996, pp.1099–1131.
Lawrence DG and Kuypers HG. The functional organization of the motor system in the monkey. I. The effects of bilateral pyramidal lesions. Brain 1968; 91: 1–14.
Lawrence DG and Kuypers HG. The functional organization of the motor system in the monkey. II. The effects of lesions of the descending brain-stem pathways. Brain 1968; 91: 15–36.
Leaw B, Nair S, Lim R, Thornton C, Mallard C, Hagberg H (2017) Mitochondria, Bioenergetics and Excitotoxicity: New Therapeutic Targets in Perinatal Brain Injury. Front Cell Neurosci 12;11:199.
Leech RW, Alvord EC. Anoxic-ischemic encephalopathy in the human neonatal period. Archives of Neurology 1977; 34:109-113.
Lequin M, Groenendaal F, Dudink J, Govaert P. Susceptibility weighted imaging can be a sensitive sequence to detect brain damage in neonates with kernicterus: a case report. BMC Neurol 2023; 23(1):104-105.
LeStrange E, Saeed N, Cowan FM, Edwards AD, Rutherford MA (2004) MR imaging quantification of cerebellar growth following hypoxic-ischemic injury in the neonatal brain. Am J Neuroradiol 25:463-468.
Leung AS, Leung EK, Paul RH. Uterine rupture after previous cesarean delivery: maternal and fetal consequences. Am J Obstet Gynecol 1993;169:945–50.
Low JA, Robertson DM and Simpson LL. Temporal relationships of neuropathologic conditions caused by perinatal asphyxia. Am J Obstet Gynecol 1989; 160: 608–614.
Macones GA, Hankins GDV, April I, Kennedy E, Shriver K. The 2008 National Institute of Child Health and Human Development workshop report on electronic fetal monitoring. Obstet Gynecol. 2008;112(3):661-666.
Malamud N. Status marmoratus : a form of cerebral palsy following either birth injury or inflammation of the central nervous system. Journal of Pediatrics 1950; 37:610-619.
Mallard EC, Waldvogel HJ, Williams CE, et al. Repeated asphyxia causes loss of striatal projection neurons in the fetal sheep brain. Neuroscience 1995; 65: 827–836.
Mallard EC, Williams CE, Gunn AJ, et al. Frequent episodes of brief ischemia sensitize the fetal sheep brain to neuronal loss and induce striatal injury. Pediatr Res 1993; 33: 61–65.
Maller AI, Hankins LL, Yeakley JW, et al. Rolandic type cerebral palsy in children as a pattern of hypoxic ischemic injury in the full-term neonate. J Child Neurol 1998; 13: 313–321.
Martin E and Barkovich AJ. Magnetic resonance imaging in perinatal asphyxia. Arch Dis Child Fetal Neonatal Ed 1995; 72: F62–F70.
Martin LJ, Brambrink A, Koehler RC, et al. Primary sensory and forebrain motor systems in the newborn brain are preferentially damaged by hypoxia-ischemia. J Comp Neurol 1997; 377: 262–285.
Martin LJ, Al-Abdulla NA, Brambrink AM, Kirsch JR, Sieber FE, Portera-Caillau C (1998) Neurodegeneration in excitotoxicity, global cerebral ischemia, and target deprivation: a perspective on the contributions of apoptosis and necrosis. Brain Research Bulletin 46:281-309.
Martin LJ, Brambrink A, Koehler RC, et al. Neonatal asphyxic brain injury is neural system preferential and targets sensory-motor networks. In: Stevenson DK and Sunshine P (eds) Fetal and neonatal brain injury: mechanisms, management and the risks of practice. Oxford: Oxford University Press, 1997, pp.374–399.
Martin LJ, Brambrink AM, Price AC, et al. Neuronal death in newborn striatum after hypoxia-ischemia is necrosis and evolves with oxidative stress. Neurobiol Dis 2000; 7: 169–191.
Martinez-Biarge M, Diez-Sebastian J, Kapellou O, Gindner D, Allsop JM,
Rutherford MA, Cowan FM. Predicting motor outcome and death in term hypoxic-ischemic encephalopathy. Neurology. 2011 Jun 14;76(24):2055-61.
Mercuri E, Guzzetta A, Haataja L, Cowan F, Rutherford M, Counsell S, Papadimitriou M, Cioni G, Dubowitz L. Neonatal neurological examination in infants with hypoxic ischaemic encephalopathy: correlation with MRI findings. Neuropediatrics. 1999 Apr;30(2):83-9.
Miller SP, Ramaswamy V, Michelson D, et al. Patterns of brain injury in term neonatal encephalopathy. J Pediatr 2005; 146: 453–460.
Misser SK, Lotz JW, van Toorn R, Mchunu N, Archary M, Barkovich AJ. Thalamus L-Sign: A Potential Biomarker of Neonatal Partial, Prolonged Hypoxic-Ischemic Brain Injury or Hypoglycemic Encephalopathy. American Journal of Neuroradiology 2022; 43(6):919-925.
Mueller-Burke D, Koehler RC and Martin LJ. Rapid NMDA receptor phosphorylation and oxidative stress precede striatal neurodegeneration after hypoxic ischemia in newborn piglets and are attenuated with hypothermia. Int J Dev Neurosci 2008; 26: 67–76.
Myers RE. Two patterns of perinatal brain damage and their conditions of occurrence. Am J Obstet Gynecol. 1972 Jan 15;112(2):246-76.
Myers RE: Atrophic cortical sclerosis associated with status marmoratus in a perinatally damaged monkey. Neurology 19:1177-1188, 1969
Myers RE and Brann AW Jr. Abruptio placentae in rhesus monkey causing brain damage to the fetus. Am J Obstet Gynecol 1976; 126: 1048–1049.
Myers RE. Experimental models of perinatal brain damage: relevance to human pathology. In: Gluck L (ed.) Intrauterine asphyxia and the developing fetal brain. Chicago: Year Book Medical, 1977, pp.37–97.
Nakajima W, Ishida A, Lange MS, Gabrielson KL, Wilson MA, Martin LJ, Blue ME, Johnston MV (2000) Apoptosis has a prolonged role in the neurodegeneration after hypoxic ischemia in the newborn rat. J Neuroscience 20(21):7994-8004.
Natale JE, Cheng Y, Martin LJ (2002) Thalamic neuronal apoptosis emerges rapidly after cortical damage in immature mice. Neuroscience 112:665-676.
Natarajan G, Pappas A, Shankaran S. Outcomes in childhood following therapeutic hypothermia for neonatal hypoxic-ischemic encephalopathy (HIE). Semin Perinatol. 2016 Dec;40(8):549-555.
Norman RM. Etat marbré of the corpus striatum following birth injury. Journal of Neurology Neurosurgery and Psychiatry 1947; 10:12-25.
Northington FJ, Ferriero DM, Graham EM, Traystman RJ, Martin LJ (2001) Early Neurodegeneration after Hypoxia-Ischemia in Neonatal Rat Is Necrosis while Delayed Neuronal Death Is Apoptosis. Neurobiology of Disease 8(2):207-19.
Northington FJ, Graham EM, Martin LJ (2005) Apoptosis in perinatal hypoxic-ischemic brain injury: how important is it and should it be inhibited ? Brain research Reviews 50:244-257.
Northington FJ, Zelaya ME, O’Riordan DP (2007) Failure to complete apoptosis following neonatal hypoxia-ischemia manifests as ‘continuum’ phenotype of cell death and occurs with multiple manifestations of mitochondrial dysfunction in rodent forebrain. Neuroscience vol. 149, no. 4, pp. 822–833.
Painter MJ (1995) Animal Models of Perinatal Asphyxia: Contributions, Contradictions, Clinical Relevance. Seminars in Pediatric Neurology, Vol2, No 1: 37-56
Papile LA, Rudolph AM and Heymann MA. Autoregulation of cerebral blood flow in the preterm fetal lamb. Pediatr Res 1985; 19: 159–161.
Parer JT, Ikeda T. A framework for standardized management of intrapartum fetal heart rate patterns. Am J Obstet Gynecol. 2007;197(1):26.e1-e6.
Parmentier CEJ, de Vries LS, Groenendaal F. Magnetic Resonance Imaging in (Near-)Term Infants with Hypoxic-Ischemic Encephalopathy. Diagnostics (Basel). 2022 Mar 6;12(3):645.
Quattrocchi CC, Fariello G and Longo D. Brainstem tegmental lesions in neonates with hypoxic-ischemic encephalopathy: magnetic resonance diagnosis and clinical outcome. World J Radiol 2016; 8: 117–123.
Ranck JB Jr, Windle WF. Brain damage in the monkey, macaca mulatta, by asphyxia neonatorum. Exp Neurol 1959; 1:130–154.
Rennie J, Rosenbloom L. How long have we got to get the baby out? A review of the effects of acute and profound intrapartum hypoxia and ischaemia. The Obstetrician & Gynaecologist 2011;13:169– 174.
Robertson RL, Ben-Sira L, Barnes PD, Mulkern RV, Robson CD, Maier SE (1999) MR line-scan diffusion-weighted imaging of term neonates with perinatal brain ischemia. AJNR Am J Neuroradiol 20(9):1658-70.
Rocha-Ferreira E, Hristova M (2016) Plasticity in the neonatal brain following hypoxic-ischaemic injury. Neural Plasticity 4901014, 1-16.
Roelants-van Rijn AM, Nikkels PG, Groenendaal F, van Der Grond J, Barth PG, Snoeck I, Beek FJ, de Vries LS. Neonatal diffusion-weighted MR imaging: relation with histopathology or follow-up MR examination. Neuropediatrics. 2001 Dec;32(6):286-94.
Roland EH, Poskitt K, Rodriguez E, et al. Perinatal hypoxic-ischemic thalamic injury: clinical features and neuroimaging. Ann Neurol 1998; 44: 161–166.
Rosenberg AA, Harris AP, Koehler RC, et al. Role of O2 -hemoglobin affinity in the regulation of cerebral blood flow in fetal sheep. Am J Physiol Heart Circ Physiol 1986; 251: H56–H62.
Rosenberg AA, Jones MD Jr., Traystman RJ, et al. Response of cerebral blood flow to changes in PCO2 in fetal, newborn, and adult sheep. Am J Physiol Heart Circ Physiol 1982; 242: H862–H866.
Rutherford, M.A., Pennock, J.M., Schwieso, J.E., Cowan, F.M., Dubowitz, L/.M.S. (1995) ‘Hypoxic ischaemic encephalopathy : early magnetic resonance imaging findings and their evolution.’, Neuropediatrics, 26, 183-191.
Rutherford M, Pennock J, Schwieso J, et al. Hypoxic-ischaemic encephalopathy: early and late magnetic resonance imaging findings in relation to outcome. Arch Dis Child Fetal Neonatal Ed 1996; 75: F145–F151.
Salas J, Reddy N, Orru E, Carson KA, Chavez-Valdez R, Burton VJ, Stafstrom CE, Northington FJ, Huisman TAGM. The Role of Diffusion Tensor Imaging in Detecting Hippocampal Injury Following Neonatal Hypoxic-Ischemic Encephalopathy. J Neuroimaging 2019; 29(2):252-259.
Sarnat H, Sarnat M. Neonatal encephalopathy following fetal distress. Arch Neurol. 33:695 - 705. 1976.
Saxon SV and Ponce CG. Behavioral defects in monkeys asphyxiated during birth. Exp Neurol 1961; 4: 460–469.
Saxon SV. Differences in reactivity between asphyxial and normal Rhesus monkeys. J Genet Psychol 1961; 99: 283–287.
Sechzer JA. Memory deficit in monkeys brain damaged by asphyxia neonatorum. Exp Neurol 1969; 24: 497–507.
Schiering IA, de Haan TR, Niermeijer JM, et al. Correlation between clinical and histologic findings in the human neonatal hippocampus after perinatal asphyxia. J Neuropathol Exp Neurol 2014; 73: 324–334.
Schneider H, Ballowitz L, Schachinger H, Hanefeld F, Dröszus J-U. Anoxic encephalopathy with predominant involvement of basal ganglia, brain stem and spinal cord in the perinatal period. Acta Neuropathologica (Berlin) 1975; 32:287-298.
Sie LT, van der Knaap MS, Oosting J, de Vries LS, Lafeber HN, Valk J. MR patterns of hypoxic-ischemic brain damage after prenatal, perinatal or postnatal asphyxia. Neuropediatrics. 2000 Jun;31(3):128-36.
Skeffington, F.S., Pearse, R.G. (1983) ‘The bright brain.’, Archives of Disease in Childhood, 58, 509-511.
Sladky JT and Rorke LB. Perinatal hypoxic/ischemic spinal cord injury. Pediatr Pathol 1986; 6: 87–101.
Slovis, T.L., Shankaran, S., Bedard, M.P. (1984) ‘Intracranial hemorrhage in the hypoxic-ischemic infant : ultrasound demonstration of unusual complications.’, Radiology, 151, 163-169.
Soul JS, Robertson RL, Tzika AA, du Plessis AJ, Volpe JJ. Time course of changes in diffusion-weighted magnetic resonance imaging in a case of neonatal encephalopathy with defined onset and duration of hypoxic-ischemic insult. Pediatrics. 2001 Nov;108(5):1211-4.
Squier W, Cowan FM (2004) The value of autopsy in determining the cause of failure to respond to resuscitation at birth. Seminars in Neonatology 9, 331-345.
Steinlin, M., Dirr, R., Martin, E., Boesch, C., Largo, R.H., Fanconi, S., Boltshauser, E. (1991) ‘MRI following severe perinatal asphyxia : preliminary experience.’, Pediatric Neurology, 7, 164-170.
Sukoff MH and Ragatz RE. Cerebellar stimulation for chronic extensor-flexor rigidity and opisthotonus secondary to hypoxia. Report of two cases. J Neurosurg 1980; 53: 391–396.
Swarte R, Lequin M, Cherian P, Zecic A, van Goudoever J, Govaert P. Imaging patterns of brain injury in term-birth asphyxia. Acta Paediatr 2009; 98(3):586-92.
Sylvester PE. Marbling and perinatal anoxia. Acta Paediatrica Scandinavica 1960; 49:338-344.
Szymonowicz W, Walker AM, Yu VY, et al. Regional cerebral blood flow after hemorrhagic hypotension in the preterm, near-term, and newborn lamb. Pediatr Res 1990; 28: 361–366.
Thompson CM, Puterman AS, Linley LL, Hann FM, van der Elst CW, Molteno CD, Malan AF. The value of a scoring system for hypoxic ischaemic encephalopathy in predicting neurodevelopmental outcome. Acta Paediatr. 1997 Jul;86(7):757-61.
Thoresen M, Jary S, Walløe L, Karlsson M, Martinez-Biarge M, Chakkarapani E, Cowan FM. MRI combined with early clinical variables are excellent outcome predictors for newborn infants undergoing therapeutic hypothermia after perinatal asphyxia. EClinicalMedicine. 2021 May 17;36:100885.
Thornton C, Hagberg H (2015) Role of mitochondria in apoptotic and necroptotic cell death in the developing brain. Clin Chim Acta 451(Pt A):35-8.
Ting P, Yamaguchi S, Bacher JD, et al. Hypoxic-ischemic cerebral necrosis in midgestational sheep fetuses: physiopathologic correlations. Exp Neurol 1983; 80: 227–245.
Tortora D, Mattei PA, Navarra R, Panara V, Salomone R, Rossi A, Detre JA, Caulo M. Prematurity and brain perfusion: Arterial spin labeling MRI. Neuroimage Clin. 2017 May 26;15:401-407.
Truttmann AC, Ginet V, Puyal J (2020) Current evidence on cell death in preterm brain injury in human and preclinical models. Front Cell Dev Biol 18; 8:27-.
Tweed WA, Cote J, Pash M, et al. Arterial oxygenation determines autoregulation of cerebral blood flow in the fetal lamb. Pediatr Res 1983; 17: 246–249.
Wagner KR, Ting P, Westfall MV, et al. Brain metabolic correlates of hypoxic-ischemic cerebral necrosis in midgestational sheep fetuses: significance of hypotension. J Cereb Blood Flow Metab 1986; 6: 425–434.
Weeke LC, Groenendaal F, Mudigonda K, Blennow M, Lequin MH, Meiners LC, van Haastert IC, Benders MJ, Hallberg B, de Vries LS. A Novel Magnetic Resonance Imaging Score Predicts Neurodevelopmental Outcome After Perinatal Asphyxia and Therapeutic Hypothermia. J Pediatr. 2018 Jan;192:33-40.e2.
Williams CE, Gunn AJ, Mallard C, Gluckman PD. Outcome after ischemia in the developing sheep brain: an electroencephalographic and histological study. Ann Neurol 1992;31:14–21.
Woolsey CN and Fairman D. Contralateral, ipsilateral, and bilateral representation of cutaneous receptors in somatic areas I and II of the cerebral cortex of pig, sheep, and other mammals. Surgery 1946; 19: 684–702.
Yuzkan S, Emecen Sanli M, Balci M, Cennetoglu P, Kafadar I, Kocak B. Use of Thalamus L-Sign to Differentiate Periventricular Leukomalacia From Neurometabolic Disorders. Journal of Child Neurology. 2023; 38(6-7):446-453.
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asphyxia: cerebral cortex: references
hippocampal dentate gyrus control versus asphyxia d9
>
Myers 1969: parasagittal cortical necrosis and status marmoratus
inferior colliculus control versus asphyxia d9
asphyxia: neuropathology in the total asphyxia model in rhesus monkeys
Ranck and WIndle 1959
The clinical presentation after this total type of asphyxia was variable. Some developed acute bilateral rigidity and then alternating flaccidity and rigidity, indicative of pathology in descending motor pathways, including corticospinal, rubrospinal, and reticulospinal tracts (Lawrence and Kuypers 1968, Lawrence and Kuypers 1968, Sukoff and Ragatz 1980, Baker 2011, Cahill-Rowley and Rose 2014) and spinal pathology. They also exhibit attenuated vestibulo-ocular and pupillary light reflexes and oral motor dysfunction, consistent with brainstem pathology (Brandt and Dieterich 1994, Quattrocchi et al. 2016). Other monkeys showed acute inability to right with diminished appendicular tone, inactivity, and hypo-responsiveness, but by six days muscle tone reappeared with paretic and ataxic walking. Other monkeys display athetoid movements, inability to right and status epilepticus.
The neuropathology at two to nine days of recovery revealed microscopic bilateral lesions throughout the neuraxis (Ranck and WIndle 1959). A pattern of selective neuronal injury primarily involved sensory nuclei, including inferior colliculus, superior olive, medial geniculate nucleus, ventral posterior thalamus, gracile and medial cuneate nuclei, vestibular nuclei, the principal sensory and motor nuclei of the trigeminal nerve. Similar brainstem and thalamic damage occurs in term human HIE (Schneider et al. 1975, Rutherford et al. 1996, de Vries and Groenendaal 2010). Some of the reduced motor activity, hypotonia, flaccidity, and depressed or absent deep tendon reflexes can be due to spinal cord injury in the human infant (Sladky and Rorke 1986). Basal ganglia damage was found in globus pallidus, the caudal half of the putamen, similar to term human HIE (Rutherford et al. 1996, de Vries and Groenendaal 2010, Martin and Barkovich 1995). Minor neuronal loss was evident in the monkey dentate gyrus, but most of the hippocampus appeared normal, unlike the vulnerability of the neonatal human hippocampus, particularly after clinical seizures (Schiering et al. 2014). Loss of Purkinje neurons was largely restricted to the vermis. Damage to the cerebral cortex involved isolated necrotic degeneration of pyramidal neurons. Seizure presence correlates with the amount of cortical necrosis in humans (Clancy et al. 1989). The HIE monkeys also exhibited white matter damage. Myelin and axonal degeneration was found in a variety of white matter tracts, including the internal capsule. Oligodendrocytes in degenerating white matter showed cytopathology (Gilles and Murphy 1969).
Of interest in this model is that the duration of asphyxial insult necessary to produce microscopic brain injury increased dramatically with decreasing gestational age, ie, 12 minutes at term compared with 30 minutes at midgestation. These findings are in accord with all other subprimate species studied.
Faro and Windle in 1969 studied another cohort (n 12) of neonatal HIE monkeys survived for 10 months to 9 years of age. Again, these monkeys showed minimal delayed damage to hippocampus. Progressive pathology was not evident in the putamen, globus pallidus or cerebellum. In contrast, the spinal cord showed atrophy of the dorsal horns and intermediolateral columns, and the brainstem pathology evolved, particularly in cochlear nuclei. The thalamus had protracted secondary pathology including the anterior ventral, ventral anterior and centromedial nuclei and the pulvinar. The primary motor and somatosensory cortices underwent apparent transneuronal degeneration and atrophy. These monkeys underwent behavioral testing during their lifetime.
Ronald Myers and coworkers extended the work in monkey HIE on over 300 term fetuses during the 1960s and 1970s (Adamsons et al. 1971, Myers 1969 and 1972, Brann and Myers 1975). Total asphyxia caused brainstem pathology; partial asphyxia led to severe edema and neocortical damage; partial asphyxia without any major increase in PCO2 or decrease in pH caused white matter injury; and partial followed by total asphyxia, as might occur during breech delivery or prolapse of the umbilical cord, induced basal ganglia damage.
neuron surrounded by macrophages in thalamus
coronal scan with 4 columns of deep grey matter damage and extensive cortical necrosis: TBG 6, CWM 6
The Rotterdam score (n=80, Swarte et al. 2009), listed below, is a derived expansion of the Barkovich et al. 1995 score. Either MR (any sequence) or ultrasound with unequivocal findings can acknowledge damage to a brain part, day 3 after birth or later, only in term infants:
- in light blue: extensive deep grey matter injury
- in green: watershed subcortical injury
- in dark blue: leukomalacia at term
- in red: isolated cortical necrosis.
Other scores were compared with each other in Langeslag et al. 2022. It is logical that the extent of damage on imaging correlates with outcome, and that MR quality is paramount. How to use these scores in redirection of care, is for several reasons, not generalisable, but scoring damage on images is essential in such decisions.
asphyxia: Rotterdam scoring system
On MRI affected deep nuclei develop a higher than normal signal intensity on T1 from day 4 to the end of the first month (or permanently), accompanied by low signal intensity on T2.
Perirolandic and peri-insular cortical highlighting (high signal on T1 and low signal on T2, especially in the depths of the sulci) is variably associated with TBG scores 3 to 6.ADC values are low even within the first day, but exceptions exist where affected nuclei have normal ADC values. ADC values normalise around the end of the first week.
In asphyxia network effects in tracts cause diffusion changes in addition to local damage of axons and collateral effects of nearby cells in thalamus and putamen. Signal inversion refers to altered signal intensity on T1 MR.
CWM cortex and white matter
PLIC posterior limb of the internal capsule
TBG thalamus and basal ganglia
Thompson et al. 1997
moderate HIE 0.1 % - handicap in 25 %
severe HIE 0.1 % - handicap in 90 %
Clinical phenotypes are arbitrarily separated into subacute partial and acute near-total type, following insights from animal studies.
Sonographic changes other than brain swelling will, as a rule, not be found after asphyxia with mild encephalopathy (Sarnat grade 1).
The group for which imaging is most relevant consists of babies with moderate encephalopathy, usually presenting with hypotonia and clinical seizures.
Criteria have been suggested to withhold the diagnosis of intrapartum asphyxia (Hankins and Speer 2003):
4 major criteria are obligatory:
- severe metabolic acidosis
- HIE = hypoxic-ischaemic encephalopathy
- later development of CP
- exclusion of other causes than intrapartum asphyxia.
At least 3 of 5 minor criteria to retain the diagnosis “intrapartum”:
- a sentinel event before or during labour
- an abnormal CTG preceded by a normal recording
- Apgar score ≤ 3 at five minutes
- multi-organ failure/ 72 h of birth
- acute brain injury on imaging.
asphyxia: criteria and clinical scores
Sarnat and Sarnat 1976
excitotoxic forebrain sensorimotor loop
management overview
An asphyxiating insult is often accompanied by a period of systemic and - when pronounced - subsequent brain hypoperfusion.
If such change is gradual there is a temporary attempt to compensate for a deficit in perfusion by redistribution of flow from the neocortex to the deep nuclei and brainstem. This leads to (sub)cortical injury, a characteristic type of which is described as the item watershed injury.
In case of arrest of perfusion there is no compensatory redistribution and deep nuclei as well as brainstem nuclei are preferentially hit. With ongoing ischaemia, and the efects of subsequent reperfusion with its molecular cascades, an increasing amount of cerebral cortex suffers primary neuronal necrosis.
Although pure presentation phenotypes of asphyxia are observed in term human neonates, the picture is often more complicated than in animal models. But the subacute type with subcortical injury and the acute total type with injury to deep grey matter, certainly exist. Thalamic neurons start to die after 10 minutes of severe bradycardia or asystoly.
the 10 min rule
neuropathology and in vivo imaging
deep grey matter injury
the complex human situation
all injury patterns
luxury perfusion
causes
stages and mechanisms
typical examples
watershed injury
rhesus monkey model
dynamics
asphyxia: cerebro-cortical injury
clinical scores
MR changes
An asphyxiating insult is often accompanied by a period of systemic and - when pronounced - subsequent brain hypoperfusion.
If such change is gradual there is a temporary attempt to compensate for a deficit in perfusion by redistribution of flow from the neocortex to the deep nuclei and brainstem. This leads to (sub)cortical injury, a characteristic type of which is described as the item watershed injury.
In case of arrest of perfusion there is no compensatory redistribution and deep nuclei as well as brainstem nuclei are preferentially hit. With ongoing ischaemia, and the efects of subsequent reperfusion with its molecular cascades, an increasing amount of cerebral cortex suffers primary neuronal necrosis.
Although pure presentation phenotypes of asphyxia are observed in term human neonates, the picture is often more complicated than in animal models. But the subacute type with subcortical injury and the acute total type with injury to deep grey matter, certainly exist. Thalamic neurons start to die after 10 minutes of severe bradycardia or asystoly.
asphyxia: evolution of fetal distress
The primary insult in birth asphyxia occurs in utero and is therefore only detailed by experimental work. The fetus moves from a compensated to a decompensated state: when oxygen delivery drops to 25-50 % acidosis develops, the metabolic rate drops and there is a gradual decline of perfusion, with (dependent on the tempo of ischaemia) redirection of blood to brainstem and diencephalon and a total body diving reflex. When oxygen delivery drops below 25 % for over 5 minutes this is followed by bradycardia, acidosis, deep hypotension, further drop in perfusion, increased carotid vascular resistance and thus ischaemia in brainstem and diencephalon. The fetus becomes very acidotic (pH < 7.0, base deficit over 20 meq/L), apnoeic, with an inactive EEG and an elevated ST segment of the ECG. Brief (< 5 min) but repetitive insults also exhaust myocardial glycogen.
after Gunn et al.
asphyxia: dynamics of management
full EEG time-synchronised
When confronted with a bad start at (near) term, there is a complicated diagnostic and therapeutic challenge for several days. Congenital anomalies and trauma are excluded by early imaging and details of the clinical history. Total body hypothermia is started on the basis of immediate criteria and on a few hours of clinical and electro-encephalographic follow-up.
Serial CUS end a day 4 or 5 MRI with diffusion sequences often provide clear views of regional injury.
CFM traces (compressed and demodulated information from a few leads)
aEEG (CFM or cerebral function monitoring) has become standard in brain monitoring until rewarming. This estimates extent of dysfunction, the need to remedy seizures and provides prognostic information that - coupled to imaging - is a basis for parental communication and in many cases an appropriate discussion about redirection of care.
asphyxia: causes
cord knot
uterine rupture
tight cord
abruptio/solutio placentae
asphyxia: biological stages
after Gunn et al. 1997 in fetal sheep model
Biological changes are separated in four stages with time from the insult on (Gunn et al. 2000).
These studies suggest that a 30-minute time frame may be :
- too long in situations when there is (near) complete obliteration of blood flow to the fetus;- too short for the management of nonacute, progressive hypoxemia for which intrauterine resuscitation measures such as maternal oxygen administration, intravenous fluids, maternal positional changes, and discontinuation of uterine stimulation may prevent the need for surgical intervention. The ongoing debate about the value of electronic fetal monitoring has focused primarily on the fact that most variant fetal heart rate (FHR) patterns are poor predictors of fetal acid–base status (Fahey 2014, Parer and Ikeda 2007, Macones et al. 2008). Attention goes to FHR patterns classified as indeterminate: neither normal nor abnormal. Given that a majority of fetuses will have an FHR pattern considered indeterminate at some point in labor, this is an important topic. It is relevant for providers to be able to recognize those patterns that signal the presence of developing acidemia and those that signal the potential presence of an acute obstetric complication that can quickly lead to acidemia and fetal asphyxia, such as a placental abruption or uterine rupture. Early identification of these FHR patterns, and immediate intervention to improve oxygenation or expedite birth, may help improve outcomes.
asphyxia: the 10 minute rule
time scale of regional damage in a carotid occlusion model in fetal sheep (Williams et al. 1992)
For obstetricians the accepted decision-to-delivery interval in the most urgent cases is 30 minutes. The evidence is that this is too slow to avoid ischaemic brain damage in a number of fetuses. Human cases of acute profound hypoxic ischaemia in which the insult duration can be timed with precision remain rare and there is often uncertainty about the prior state of fetal health. While there is clear variability both in the fetal reserve and in the duration and degree of the insult, we think that that damage begins to accrue after 10 minutes of an acute profound hypoxic ischaemic insult (Rennie and Rosenbloom 2011).
In monkeys near term, anaesthetised with isoflurane, the umbilical cord was exteriorised and then clamped for 12–15 minutes. The animals were subsequently delivered by caesarean section, resuscitated with positive pressure ventilation, and studied with EEG and MRI in the neonatal period (Juul et al. 2007). After 15 minutes of clamping, the umbilical cord pH was 6.86 with a base deficit of 23 mmol/l and the animals took between 13–30 minutes to take their first breath. 12 Minutes did not produce a reliably severe insult using this model, whereas 15 minutes did. Results confirm the very short time between no damage and damage: after 15 minutes of clamping 100% of these animals had significant brain injury.
In a retrospective study of 106 human cases of uterine rupture between 1983 and 1992, fetuses exposed to prolonged deceleration could survive without asphyxia if they were delivered before 17 minutes had elapsed, but several babies developed neonatal morbidity after 10 minutes of a prolonged deceleration if there had been previous late decelerations (range 36–90 minutes)(Leung et al. 1993).
asphyxia: luxury perfusion in the arterial compartment
It is unlikely for arterial perfusion indices to add substantially to prognostication, in individual cases, when the injury pattern has been well defined by imaging.
In the acute stage at least three mechanisms interfere to disrupt the interaction between thalamus, cortex and striatum.
1. Following the insult OFR damage occurs in neurons of thalamus and cortex rich in mitochondria, this is the primary insult.
2. Cortical dysfunction and primary injury to striatal neurons will disinhibit thalamus that is normally inhibited by the striatum. There is a loop of thalamocortical inappropriate activation.
3. WIthin hours to days, neurons in thalamus that need trophic support from the cortex, will wither.
Dyskinetic cerebral palsy follows destruction of pallidal and subthalamic functional stations in the striatum.
A disinhibiton of thalamus by injury to striatum leads to hypertonia and dystonia, but injury to thalamus itself interferes with the clinical outcome, in a manner not really understood in the era of hypothermia facing mitigated injury of several components in the loops.
asphyxia: excitotoxic and trophic damage in sensorimotor forebrain systems
asphyxia: major injury patterns
asphyxia: cortical injury
R
<—— insular cortical necrosis
P
cystic end stage
caudate head ——>
insular and cingulate cortex
A
<—— cortical necrosis
deep grey and cortical
postrolandic 1
cortical necrosis ——>
GP
Injury to neurons is clearly demarcated by this haemorrhagic conversion, also in amygdala A, septum and rolandic cortex R. T2 MRI on day 4. Notice sparing of the caudate head.
haemorrhagic necrosis
postrolandic 2
P
L
I
C
bright brain preterm
<—— putamen
insular cortex
T
maturation
<—— thalamus
—>
term asphyxia without sentinel event; selective cortical injury in insular gyri (right parasagittal T1), referred to as cortical highlighting
Selective neuronal necrosis (often with karyorrhexis) in cerebral cortex, hippocampus (subiculum and H1) and internal cerebellar granular layer, is the most important postmortem finding in asphyxiated term newborns with status epilepticus (Larroche 1968, Friede 1989). All brain lobes can be affected, gyri in their crowns and in sulcal depths. Total necrosis is seen next to laminar and patchy necrosis ('en flammèches'), glial and vascular reaction is minimal. Cerebral cortical cell death is seen with the deep grey matter and brainstem paradigm of injury and also with watershed injury. It can also be a pattern of its own. A similar pattern has been observed in infants following apparent life-threatening events. These changes represent a severe form of selective neuronal necrosis, evolving towards (sub)cortical cystic parenchymal necrosis. Ventriculomegaly is often associated even before cysts appear.
The imaging correlate of pontosubicular necrosis, an histopathogical entity repeatedly described in relation to hypoxia, has not yet been defined.On diffusion weighted MR sequences the affected areas may be restricted (rolandic, cingulate, calcarine, insular) or very extensive. In the latter the appearance on diffusion sequences has been referred to as the bright brain, entire cerebral cortex lighting up in contrast to “normal” cerebellar cortex. On occasion (at least in some with acute hypovolaemia due to blood loss) a purely postrolandic pattern of cortical necrosis occurs.
In a fetal sheep model (and also in human practice) laminar cortical necrosis is preceded by EEG depression for about 8 hours, followed by acute transition to low-frequency epileptiform activity that gradually regresses over 72 hours (Williams et al. 1992). The peak of epileptic activity coincides with brain swelling.
neuropathology and imaging of primary cortical necrosis
Using CUS, a pattern other than white matter hyperechogenicity may precede (sub)cortical cyst formation in the late first and second post-insult week. Sonographic “maturation” of the pattern seems slower than for deep grey matter, especially in cooled infants. One may suspect cortical ischaemia when finding hyperechoic zones around sulci in contrast to the ‘railroad tracks’ that are so characteristic of hyperechoic change in white matter. An hyperechoic band of variable width stretches out starting from the bright line of a sulcus or fissure and can be distinguished from less echoic healthy white matter. Sulcus and cortex, with a variable border of subcortical white matter, tend to merge into one echoic zone, consisting of minute bright dots that follow the sulcus curvature (a collection of echobright lainae). The thickness of these laminae may vary, thinner ones being composed of spiculae with decreasing density away from the sulcus; even thin bands may still end with cystic necrosis.
This pattern of laminar cortical hyperechogenicity is not uncommon. The neat separation between this ‘cortical’ picture and gyral core hyperechogenicity deserves emphasis especially in view of the potentially similar end result: cystic necrosis in the frontoparietal lobes. Such observation stresses the importance — if death occurs — of making every effort to correlate sequential CUS appearance with postmortem analysis (see Eken et al. 1994).
The term laminar cortical necrosis may not be appropriately used here because it is already in use by histopathologists to describe selective necrosis in the lower layers of the cortical plate following ischaemic incidents.
intrapartum twin to twin transfusion with acute hypovolaemia in this twin, not cooled; diffusion sequence with bright cerebrum on day 4
Normal neonatal cortex intensity on MR (up to ≈ 3 mo):
- short T1 (brighter) and short T2 (darker), with longer white matter T1 and T2 → obvious cortex/white matter differentiation
- gradual prolongation of cortical values causes loss of differentiation near 3 months post term
- cortical highlighting by HIE and changes in white matter signal intensity were well documented in early research on this topic
- references to diffusion imaging in asphyxia: Soul et al. 2001, Barkovich et al. 2006, Swarte et al. 2009, Imai et al. 2018, Annink et al. 2020)
asphyxia: signal intensity changes on MRI following term birth asphyxia
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