Corpus Callosum Size in Relation to Motor Performance in 9- to 10-Year-Old Children with Neonatal Encephalopathy

Kooij, Britt J.M. van; Handel, M; Uiterwaal, Cuno S.P.M.; Groenendaal, Floris; Nievelstein, Rutger A.J.; Rademaker, Karin J; Jongmans, Marian J.; Vries, Linda S. de

doi:10.1203/pdr.0b013e31815b4435

Cited by 37 publications

(26 citation statements)

References 32 publications

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“…The thickness of the corpus callosum can be influenced by a deficit in myelination and/or axonal damage. In human neonates, a reduction in corpus callosum thickness is associated with cognitive and motor impairment [48,49,50]. Additionally, arborization of the myelinated fibers in the cingulum was strongly reduced by LPS+HI.…”

Section: Discussionmentioning

confidence: 99%

Development of Cerebral Gray and White Matter Injury and Cerebral Inflammation over Time after Inflammatory Perinatal Asphyxia

Bonestroo¹,

Heijnen²,

Groenendaal

et al. 2015

Dev Neurosci

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Antenatal inflammation is associated with increased severity of hypoxic-ischemic (HI) encephalopathy and adverse outcome in human neonates and experimental rodents. We investigated the effect of lipopolysaccharide (LPS) on the timing of HI-induced cerebral tissue loss and gray matter injury, white matter injury and integrity, and the cerebral inflammatory response. On postnatal day 9, mice underwent HI by unilateral carotid artery occlusion followed by systemic hypoxia which resulted in early neuronal damage (MAP2 loss) at 3 h that did not increase up to day 15. LPS injection 14 h before HI (LPS+HI) significantly and gradually aggravated MAP2 loss from 3 h up to day 15, resulting in an acellular cystic lesion. LPS+HI increased white matter damage, reduced myelination in the corpus callosum and increased white matter fiber coherency in the cingulum. The number of oligodendrocytes throughout the lineage (Olig2-positive) was increased whereas more mature myelinating (CNPase-positive) oligodendrocytes were strongly decreased after LPS+HI. LPS+HI induced an increased and prolonged expression of cerebral cytokines/chemokines compared to HI. Additionally, LPS+HI increased macrophage/microglia activation and influx of neutrophils in the brain compared to HI. This study demonstrates the sensitizing effect of LPS on neonatal HI brain injury for an extended time-frame up to 15 days postinsult. LPS before HI induced a gradual increase in gray and white matter deficits, including reduced numbers of more mature myelinating oligodendrocytes and a decrease in white matter integrity. Moreover, LPS+HI prolonged and intensified the cerebral inflammatory response, including cellular infiltration. In conclusion, as the timing of damage and/or involved pathways are changed when HI is preceded by inflammation, experimental therapies might require modifications in the time window, dosage or combinations of therapies for efficacious neuroprotection.

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Section: Discussionmentioning

confidence: 99%

Development of Cerebral Gray and White Matter Injury and Cerebral Inflammation over Time after Inflammatory Perinatal Asphyxia

Bonestroo¹,

Heijnen²,

Groenendaal

et al. 2015

Dev Neurosci

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“…They more often developed CP and more often attended special education. In a subgroup (n=61) of the same cohort and in 47 controls the area of the corpus callosum (CC) was measured and related to the Movement ABC test score 51. Children with moderate NE had significantly smaller middle and posterior parts and total areas of the CC.…”

Section: Long-term Outcome In Later Childhood and Adolescencementioning

confidence: 99%

Long-term outcome after neonatal hypoxic-ischaemic encephalopathy

Vries

Jongmans

2010

Archives of Disease in Childhood - Fetal and Neonatal Edition

209

140

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Outcome of full-term infants with neonatal encephalopathy of hypoxic-ischemic origin is often assessed in infancy or early childhood and data on outcome in childhood and adolescence is limited. MRI performed in the neonatal period has made a huge contribution to recognition of different patterns of injury. These different patterns of injury are related to the severity of later motor and cognitive disabilities.Long-term follow-up shows that cognitive and memory diffi culties may follow even in children without motor defi cits. It is therefore recommended to perform follow-up assessment into childhood in children with and without adverse neurological outcome in early infancy.Neonatal encephalopathy (NE) occurs in 1-6/1000 live full-term births and carries a high risk for subsequent neurodevelopmental disabilities. 1 Longterm outcome is known to depend on the severity of the neonatal condition. 2 3 The term NE is now more often used than perinatal asphyxia (PA). This is because PA is diffi cult to defi ne and in order to be reliable, needs access to several markers which are not always available, such as fetal heart rate tracings, umbilical cord gases and reliable Apgar scores. Individually, these markers have been shown to not correlate very well with subsequent outcome. 4 5 NE is 'a clinically defi ned syndrome of disturbed neurological function in the earliest days of life in the full-term infant, manifested by diffi culty with initiating and maintaining respiration, depression of tone and refl exes, subnormal level of consciousness and often seizures'. The widely used three-level grading system of mild, moderate and severe encephalopathy, based on clinical symptoms and EEG, was developed by Sarnat and Sarnat. 6 They based their encephalopathy score on an assessment in only 21 infants. The development of encephalopathy in full-term infants within hours to days after birth is now considered essential in order to be confi dent about an underlying perinatal insult, and NE is almost invariably associated with several of the markers mentioned above. 7 NE can develop for reasons other than hypoxic-ischaemia, for example, metabolic disorders, therefore a combination of markers suggestive of the presence of PA as well as the development of NE is obligatory.Most studies reported so far have focused on early neurodevelopmental outcome at 18-24 months, looking mainly at development of cerebral palsy (CP) or severe cognitive defi cits. 8 Outcome of infants with mild NE have been reported to be comparable to non-affected full-term infants, 2 9 while those with severe NE will either die or

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“…Through adulthood and the aging process, reductions in size are noted (Allen et al, 1991;Smith et al, 2007). Furthermore, callosal size and area are associated with motor skills and numerous cognitive abilities (Fine et al, 2007;Hutchinson et al, 2009;Rademaker et al, 2004;van Kooij et al, 2008), and the corpus callosum is often malformed or absent in various conditions (Jeret et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Age-related regional variations of the corpus callosum identified by diffusion tensor tractography

Lebel

Caverhill-Godkewitsch

2010

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Corpus Callosum Size in Relation to Motor Performance in 9- to 10-Year-Old Children with Neonatal Encephalopathy

Cited by 37 publications

References 32 publications

Development of Cerebral Gray and White Matter Injury and Cerebral Inflammation over Time after Inflammatory Perinatal Asphyxia

Development of Cerebral Gray and White Matter Injury and Cerebral Inflammation over Time after Inflammatory Perinatal Asphyxia

Long-term outcome after neonatal hypoxic-ischaemic encephalopathy

Age-related regional variations of the corpus callosum identified by diffusion tensor tractography

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