Plasticity in the Neonatal Brain following Hypoxic-Ischaemic Injury
Hypoxic-ischaemic damage to the developing brain is a leading cause of child death, with high mortality and morbidity, including cerebral palsy, epilepsy, and cognitive disabilities. The developmental stage of the brain and the severity of the insult influence the selective regional vulnerability an...
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| Format: | Article |
| Language: | English |
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Wiley
2016-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2016/4901014 |
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| author | Eridan Rocha-Ferreira Mariya Hristova |
| author_facet | Eridan Rocha-Ferreira Mariya Hristova |
| author_sort | Eridan Rocha-Ferreira |
| collection | DOAJ |
| description | Hypoxic-ischaemic damage to the developing brain is a leading cause of child death, with high mortality and morbidity, including cerebral palsy, epilepsy, and cognitive disabilities. The developmental stage of the brain and the severity of the insult influence the selective regional vulnerability and the subsequent clinical manifestations. The increased susceptibility to hypoxia-ischaemia (HI) of periventricular white matter in preterm infants predisposes the immature brain to motor, cognitive, and sensory deficits, with cognitive impairment associated with earlier gestational age. In term infants HI causes selective damage to sensorimotor cortex, basal ganglia, thalamus, and brain stem. Even though the immature brain is more malleable to external stimuli compared to the adult one, a hypoxic-ischaemic event to the neonate interrupts the shaping of central motor pathways and can affect normal developmental plasticity through altering neurotransmission, changes in cellular signalling, neural connectivity and function, wrong targeted innervation, and interruption of developmental apoptosis. Models of neonatal HI demonstrate three morphologically different types of cell death, that is, apoptosis, necrosis, and autophagy, which crosstalk and can exist as a continuum in the same cell. In the present review we discuss the mechanisms of HI injury to the immature brain and the way they affect plasticity. |
| format | Article |
| id | doaj-art-5d635fb391fb4cd4b5391c3db7792ea3 |
| institution | Kabale University |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2016-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-5d635fb391fb4cd4b5391c3db7792ea32025-08-20T03:34:45ZengWileyNeural Plasticity2090-59041687-54432016-01-01201610.1155/2016/49010144901014Plasticity in the Neonatal Brain following Hypoxic-Ischaemic InjuryEridan Rocha-Ferreira0Mariya Hristova1UCL Institute for Women’s Health, Maternal & Fetal Medicine, Perinatal Brain Repair Group, London WC1E 6HX, UKUCL Institute for Women’s Health, Maternal & Fetal Medicine, Perinatal Brain Repair Group, London WC1E 6HX, UKHypoxic-ischaemic damage to the developing brain is a leading cause of child death, with high mortality and morbidity, including cerebral palsy, epilepsy, and cognitive disabilities. The developmental stage of the brain and the severity of the insult influence the selective regional vulnerability and the subsequent clinical manifestations. The increased susceptibility to hypoxia-ischaemia (HI) of periventricular white matter in preterm infants predisposes the immature brain to motor, cognitive, and sensory deficits, with cognitive impairment associated with earlier gestational age. In term infants HI causes selective damage to sensorimotor cortex, basal ganglia, thalamus, and brain stem. Even though the immature brain is more malleable to external stimuli compared to the adult one, a hypoxic-ischaemic event to the neonate interrupts the shaping of central motor pathways and can affect normal developmental plasticity through altering neurotransmission, changes in cellular signalling, neural connectivity and function, wrong targeted innervation, and interruption of developmental apoptosis. Models of neonatal HI demonstrate three morphologically different types of cell death, that is, apoptosis, necrosis, and autophagy, which crosstalk and can exist as a continuum in the same cell. In the present review we discuss the mechanisms of HI injury to the immature brain and the way they affect plasticity.http://dx.doi.org/10.1155/2016/4901014 |
| spellingShingle | Eridan Rocha-Ferreira Mariya Hristova Plasticity in the Neonatal Brain following Hypoxic-Ischaemic Injury Neural Plasticity |
| title | Plasticity in the Neonatal Brain following Hypoxic-Ischaemic Injury |
| title_full | Plasticity in the Neonatal Brain following Hypoxic-Ischaemic Injury |
| title_fullStr | Plasticity in the Neonatal Brain following Hypoxic-Ischaemic Injury |
| title_full_unstemmed | Plasticity in the Neonatal Brain following Hypoxic-Ischaemic Injury |
| title_short | Plasticity in the Neonatal Brain following Hypoxic-Ischaemic Injury |
| title_sort | plasticity in the neonatal brain following hypoxic ischaemic injury |
| url | http://dx.doi.org/10.1155/2016/4901014 |
| work_keys_str_mv | AT eridanrochaferreira plasticityintheneonatalbrainfollowinghypoxicischaemicinjury AT mariyahristova plasticityintheneonatalbrainfollowinghypoxicischaemicinjury |