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Results for “Prenatal Injuries”

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At least 37 records · Page 2Linked to original sources
PubMed2006

Law, pregnancy and sport: what are the repercussions when a pregnant lady plays?

This article reflects on the issue of pregnancy and sport that was brought to the fore in Gardner v National Netball League (2001) 182 ALR 408; [2001] FMCA 50 and Gardner v All Australia Netball Association Ltd (2003) 174 FLR 452. It suggests that these cases did not provide a definitive discussion of the tortious liability implications that initially led Netball Australia to introduce a ban on pregnant players. In an attempt to fill some of these gaps, other case law that deals with liability of sporting organisations and prenatal injury is discussed. The article primarily focuses on whether the unborn child when born alive will have an action against her or his mother as a result of injury occasioned while the mother was playing sport when pregnant. This examination is undertaken in light of recent Australian tort reform as well as changes in policy direction. The article summarises the legal position of the parties involved in sport--sporting organisations, medical practitioners, other participants and the pregnant mother--and argues that, with reference to the guidelines and case law, in only a very small number of cases would liability be found against the sporting organisation or pregnant mother as a result of injuries incurred prenatally.

Australia↗
PubMed2001

Mechanisms of brain injury: L1 cell adhesion molecule as a target for ethanol-induced prenatal brain injury.

The magnitude of the problem of neurodevelopmental disorders is enormous. Frequently, the mechanism of injury is unknown. In this article, the function of one cell adhesion molecule, L1, will be reviewed. L1 is critical for proper central nervous system development. Similarities between patients with fetal alcohol syndrome and with L1 mutations suggest that the mechanism of developmental neurotoxicity of ethanol is partly due to effects on L1 cell adhesion molecule.

Adult↗
PubMed2004

Cell death in the rat hippocampus in a model of prenatal brain injury: time course and expression of death-related proteins.

Survival rates have increased dramatically for very premature (gestational week 24-28) infants. However, many of these infants grow up to have profound cognitive, motor and behavioral impairments due to brain damage. We have developed a novel model of prenatal infant gray matter injury. During the neonatal period, GABA is an excitatory neurotransmitter. GABA(A) receptor activation results in chloride efflux and membrane depolarization sufficient to open L-type voltage sensitive calcium channels. Our model involves excessive GABA(A) receptor activation in the newborn rat, with damage due to the resultant excessive calcium influx, not GABA(A) receptor activation itself. A common feature among numerous insult pathologies in the neonatal brain is an elevation in the intracellular levels of calcium. The goals of the present study were: 1) to document the time course and amount of cell death (both apoptotic and necrotic), and 2) to investigate the effect of GABA(A) receptor activation on the time course and expression of three cell death-related proteins (caspase-9, bax and bcl-2) in our model of prenatal brain injury. The magnitude of cell death, using TdT-mediated dUTP nick end labeling and Cresyl Violet to quantify the incidence of apoptotic and necrotic cells, was region dependent (CA1>CA2/3>dentate gyrus) and persisted for at least 5 days following insult. There was a relative increase in the amount of bax to bcl-2 protein, and increased protein levels of caspase-9, indicative of cell death. These findings are consistent with mechanisms of cell death seen in other types of early brain insult, and highlight a conserved cascade of events leading to cell death in the developing brain.

Animals↗
PubMed2003

Alternative brain organization after prenatal cerebral injury: convergent fMRI and cognitive data.

The current study presents both longitudinal behavioral data and functional activation data documenting the effects of early focal brain injury on the development of spatial analytic processing in two children, one with prenatal left hemisphere (LH) injury and one with right hemisphere (RH) injury. A substantial body of evidence has shown that adults and children with early, lateralized brain injury show evidence of spatial analytic deficits. LH injury compromises the ability to encode the parts of a spatial pattern, while RH injury impairs pattern integration. The two children described in this report show patterns of deficit consistent with the site of their injury. In the current study, their longitudinal behavioral data spanning the age range from preschool to adolescence are presented in conjunction with data from a functional magnetic resonance imaging (fMRI) study of spatial processing. The activation results provide evidence that alternative profiles of neural organization can arise following early focal brain injury, and document where in the brain spatial functions are carried out when regions that normally mediate them are damaged. In addition, the coupling of the activation with the behavioral data allows us to go beyond the simple mapping of functional sites, to ask questions about how those sites may have come to mediate the spatial functions.

Adolescent↗
PubMed1999

Fetal thrombotic vasculopathy in the placenta: cerebral thrombi and infarcts, coagulopathies, and cerebral palsy.

Thrombi in the fetal circulation of the placenta cause a pattern of clustered fibrotic villi called fetal thrombotic vasculopathy (FTV), which has been associated with serious injuries to neonates, especially brain injuries. Correlation of FTV with visceral thrombi in autopsy specimens might lead to a more accurate estimate of the prevalence of somatic thrombi as a significant and underrecognized cause of prenatal injury or perinatal death, and show the potential validity of placental FTV as an indicator of thrombotic lesions in the fetus and newborns who survive. Clinicopathologic correlation was used to perform a 3-year retrospective autopsy review. We identified 16 cases (19%) among 84 perinatal autopsy specimens in which placental FTV was associated with stillbirth, intrapartum, or neonatal death. Two liveborn neonates survived 2.5 hours, and one for 24 hours; there was one intrapartum death, and the rest were stillborn. Clinical evidence of severe central nervous system (CNS) injury to two of the liveborn infants was evident at birth. Twelve stillborns died from 12 to 48 hours before delivery. Placental FTV had features of organization that clearly antedated the fetal death. Autopsy findings confirmed somatic thrombi in six cases (37.5%) of the 16 with FTV, including cerebral thrombi or infarcts (three cases), renal thromboemboli (three cases), and pulmonary thromboemboli (two cases). One mother had history of deep vein thrombosis, and four of eight tested had abnormal coagulation test results. Placental FTV indicates a significant probability of thrombi in the fetus and represents an important, possibly underrecognized cause of perinatal mortality and neonatal injury. Parental coagulopathy as a significant factor in prenatal injury and death deserves more comprehensive study. The placenta remains an undervalued and underutilized surgical specimen in the evaluation of perinatal injury, especially cerebral palsy.

Blood Coagulation Disorders↗
PubMed1991

The incidence of prenatal brain injury.

Recent epidemiological studies have shown that cerebral palsy is only rarely associated with birth asphyxia and that there may be more important causative factors in the prenatal period. For this reason a series of 165 brains of infants who were stillborn or died in the early neonatal period was examined in order to identify the incidence and nature of prenatal brain damage. Seventeen (44%) of the stillborn infants showed evidence of brain damage thought to be related to circulatory disorders. The most frequent abnormality, widespread ischaemic damage to the white matter of the cerebral hemispheres, occurred in 10 (26%). Criteria for white matter ischaemia were reactive astrocytosis, macrophage infiltration, karyorrhexis and endothelial swelling or reduplication. This abnormality was only seen after 27 weeks gestation. In five (13%) of the stillborn infants, haemorrhage was seen in association with ischaemic damage and in only two (5%) did brain haemorrhage occur in utero without evidence of co-existing ischaemic damage. Of the 90 live-born infants, 12 (16%) of those surviving less than 3 days and three (20%) of 15 infants who lived between 3 and 7 days after birth showed ischaemic damage which was of prenatal origin. The most frequent pathological change in the infants studied was white matter gliosis occurring in infants who survived into or beyond the last trimester. This may interfere with normal myelination by diverting glial stem cells into reactive astrocytes and thus reduce the population of oligodendrocytes available to synthesize myelin and so cause permanent neurological damage.

Abortion, Spontaneous↗
PubMed2002

[Focal cortical dysplasia possibly related to a probable prenatal ischemic injury].

Focal cortical dysplasias are a frequent etiology of partial seizure disorders refractory to medical treatment. We report the case of a patient with focal cortical dysplasia, confirmed by surgery, in association with ischemic cerebral lesions that possibly occurred during the intra-uterine development. This observation reinforces the hypothesis of a possible factor of causality between prenatal ischemia and anomalies of cortical development.

Anticonvulsants↗