“…17 In a large cohort of extremely low birth weight infants, those with Papile grade 3 intraventricular hemorrhage who required a shunt were at twice the risk of cerebral palsy compared to those who did not. 18 A likely intermediate is white matter damage 19 which was associated with intraventricular hemorrhage in the present study. To the extent that intraventricular hemorrhage is causally related to white matter damage, it very likely is an important antecedent of developmental impairments, particularly cerebral palsy.…”
Whether intraventricular hemorrhage increases the risk of adverse developmental outcome among premature infants is controversial. Using brain ultrasound, we identified IVH and white matter abnormalities among 1064 infants born before 28 weeks gestation. We identified adverse developmental outcomes at 24 months of age using a standardized neurological examination and the Bayley Scales of Infant Development Mental and Motor Scales. In logistic regression models that adjusted for gestational age, sex, and public insurance, isolated intraventricular hemorrhage was associated with visual fixation difficulty (odds ratio: 2.5 (95% confidence limits: 1.2, 5.1)) but no other adverse outcome. Infants who had a white matter lesion unaccompanied by intraventricular hemorrhage were at increased risk of cerebral palsy, low Mental and Motor Scores, and visual and hearing impairments. Except when accompanied or followed by a white matter lesion, intraventricular hemorrhage is associated with no more than a mild increase (and possibly no increase) in the risk of adverse developmental outcome during infancy.
“…17 In a large cohort of extremely low birth weight infants, those with Papile grade 3 intraventricular hemorrhage who required a shunt were at twice the risk of cerebral palsy compared to those who did not. 18 A likely intermediate is white matter damage 19 which was associated with intraventricular hemorrhage in the present study. To the extent that intraventricular hemorrhage is causally related to white matter damage, it very likely is an important antecedent of developmental impairments, particularly cerebral palsy.…”
Whether intraventricular hemorrhage increases the risk of adverse developmental outcome among premature infants is controversial. Using brain ultrasound, we identified IVH and white matter abnormalities among 1064 infants born before 28 weeks gestation. We identified adverse developmental outcomes at 24 months of age using a standardized neurological examination and the Bayley Scales of Infant Development Mental and Motor Scales. In logistic regression models that adjusted for gestational age, sex, and public insurance, isolated intraventricular hemorrhage was associated with visual fixation difficulty (odds ratio: 2.5 (95% confidence limits: 1.2, 5.1)) but no other adverse outcome. Infants who had a white matter lesion unaccompanied by intraventricular hemorrhage were at increased risk of cerebral palsy, low Mental and Motor Scores, and visual and hearing impairments. Except when accompanied or followed by a white matter lesion, intraventricular hemorrhage is associated with no more than a mild increase (and possibly no increase) in the risk of adverse developmental outcome during infancy.
“…However, the results of our study and those of Kuban et al (1999) suggest that the combination of VD and associated GMH-IVH on neonatal cranial ultrasound may provide a useful surrogate marker of (subtle) white matter injury in the neonatal period.…”
This study investigated whether in preterm children who had ventricular dilatation (VD) on neonatal cranial ultrasound outcome at age 8 years was influenced by the additional presence of germinal matrix haemorrhage -intraventricular haemorrhage (GMH-IVH). Six-hundred and ninety-nine preterm infants (<33wks' gestation, mean 29.6wks [SD 2.1]) with either normal cranial ultrasound (n=616; 286 females, 330 males), or with VD with (n=66; 32 females, 34 males) or without (n=17; 4 females, 13 males) GMH-IVH were enrolled in the study. At age 8 years outcome was assessed in 567 (81%) of the 699 children by neurological examination, the Test of Motor Impairment (TOMI), the test of Visuo-Motor Integration (VMI), and the Wechsler Intelligence Scales for Children. Results showed that the proportion of children with disabling impairments was higher in the group with VD and GMH-IVH. Performance on TOMI and VMI (even in those without disabling impairments) was poorer in those with VD and GMH-IVH than in children with normal scans or those with VD only. Children with VD and GMH-IVH had significantly lower performance IQ than children with normal ultrasound, whereas those with VD only were not different from those with normal scans. Results suggest the presence of subtle white matter injury that has not been identified by neonatal cranial ultrasound. Although this study did not investigate biochemical markers of haemorrhage, we hypothesize that non-proteinbound iron is likely to be a contributing factor to white matter damage in preterm infants.
“…1 A total of 520 neonates r32 weeks in GA were admitted over the 2 1 2 years study period ( Figure 1) F overall, 41 had no HUS (16 died before a scan was done), 379 had normal (or only minor abnormality) studies, and 100 (21% of all those scanned) had major HUS abnormalities detected (Table 1), comparable to previous reports. [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15] We excluded from further analysis the 41 babies having no HUS study, the 198 having only one study, and 40 infants who had two studies, but less than 7 days apart (the 20 normal infants from this group had no repeat scans). Of the remaining 241 infants who had two or more scans, with the first two Z7 days apart, 43 were abnormal on the first or second study, with six of these reverting to normal on a third scan.…”
Section: Methodsmentioning
confidence: 99%
“…9,10 Infants with the earliest onset of hemorrhage may have extension subsequently, and may later develop posthemorrhagic hydrocephalus, VM, and/or PVL. [9][10][11] The reported incidence of PVL varies from 3 to 15%. 12,13 On HUS, PVL may initially appear as increased periventricular white matter echogenicity that subsequently evolves into leukomalacia and/or cyst formation 1 to 3 weeks later.…”
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