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White Matter Damage (white + matter_damage)
Selected AbstractsHistological and Ultrastructural Analysis of White Matter Damage after Naturally-occurring Spinal Cord InjuryBRAIN PATHOLOGY, Issue 2 2006Peter M. Smith Detailed analysis of the structural changes that follow human clinical spinal cord injury is limited by difficulties in achieving adequate tissue fixation. This study bypasses this obstacle by examining the spinal cord from paraplegic domestic animals, enabling us to document the ultrastructural changes at different times following injury. In all but one case, injury resulted from a combination of contusion and compression. There was infarction and hemorrhage, followed by gray matter destruction and the rapid development of a variety of white matter changes including axon swelling and myelin degeneration. Axons greater than 5 µm in diameter were more susceptible to degenerative changes, whereas smaller axons, particularly those in the subpial region, were relatively well preserved. Demyelinated axons were seen within 2 weeks after injury and, at later time points, both Schwann cell and oligodendrocyte remyelination was common. More subtle white matter abnormalities were identified by examining sagittal sections, including focal accumulation of organelles in the axoplasm and partial and paranodal myelin abnormalities. These observations serve to validate observations from experimental models of spinal contusion but also highlight the complexity of naturally occurring (ie, clinical) spinal injury. They also raise the possibility that focal abnormalities such as paranodal demyelination may contribute to early axonal dysfunction and possibly to progressive tissue damage. [source] Gestational Hypoxia Induces White Matter Damage in Neonatal Rats: A New Model of Periventricular LeukomalaciaBRAIN PATHOLOGY, Issue 1 2004Olivier Baud In the premature infant, periventricular leukomalacia, usually related to hypoxic-ischemic white matter damage, is the main cause of neurological impairment. We hypothesized that protracted prenatal hypoxia might induce white matter damage during the perinatal period. Pregnant Sparague-Dawley rats were placed in a chamber supplied with hypoxic gas (10% O2 -90% N2) from embryonic day 5(E5) to E20. Neonatal rat brains were investigated by histology, immunocytochemistry, western blotting, in situ hybridization, DNA fragmentation analysis, and in vivo magnetic resonance imaging (MRI). Body weight of pups subjected to prenatal hypoxia was 10 to 30% lower from p0 to P14 than in controls. Specific white matter cysts wear detected between p0 and p7 in pups subjected to prenatal hypoxia, in addition to abnormal extra-cellular matrix, increased lipid peroxidation, white matter cell death detected by TUNEL and increased activated macrophage counts in white matter. Subsequently, gliotic scars and delayed myelination primarily involving immature oligodendrocytes were seen In vivo MRI with T1, T2, and diffusion sequences disclosed similar findings immediately after birth, showing strong correlations with histological abnormalities. We speculate that protracted prenatal hypoxia in rat induces abnormalities. We speculate that protracted prenatal hypoxia in rat induces white matter damage occurring through local inflammatory response and oxidative stress linked to re-oxygenation during the perinatal period. [source] Models of white matter injury: Comparison of infectious, hypoxic-ischemic, and excitotoxic insultsDEVELOPMENTAL DISABILITIES RESEARCH REVIEW, Issue 1 2002Henrik Hagberg Abstract White matter damage (WMD) in preterm neonates is strongly associated with adverse outcome. The etiology of white matter injury is not known but clinical data suggest that ischemia-reperfusion and/or infection-inflammation are important factors. Furthermore, antenatal infection seems to be an important risk factor for brain injury in term infants. In order to explore the pathophysiological mechanisms of WMD and to better understand how infectious agents may affect the vulnerability of the immature brain to injury, numerous novel animal models have been developed over the past decade. WMD can be induced by antenatal or postnatal administration of microbes (E. coli or Gardnerella vaginalis), virus (border disease virus) or bacterial products (lipopolysaccharide, LPS). Alternatively, various hypoperfusion paradigms or administration of excitatory amino acid receptor agonists (excitotoxicity models) can be used. Irrespective of which insult is utilized, the maturational age of the CNS and choice of species seem critical. Generally, lesions with similarity to human WMD, with respect to distribution and morphological characteristics, are easier to induce in gyrencephalic species (rabbits, dogs, cats and sheep) than in rodents. Recently, however, models have been developed in rats (PND 1,7), using either bilateral carotid occlusion or combined hypoxia-ischemia, that produce predominantly white matter lesions. LPS is the infectious agent most often used to produce WMD in immature dogs, cats, or fetal sheep. The mechanism whereby LPS induces brain injury is not completely understood but involves activation of toll-like receptor 4 on immune cells with initiation of a generalized inflammatory response resulting in systemic hypoglycemia, perturbation of coagulation, cerebral hypoperfusion, and activation of inflammatory cells in the CNS. LPS and umbilical cord occlusion both produce WMD with quite similar distribution in 65% gestational sheep. The morphological appearance is different, however, with a more pronounced infiltration of inflammatory cells into the brain and focal microglia/macrophage ("inflammatory WMD") in response to LPS compared to hypoperfusion evoking a more diffuse microglial response usually devoid of cellular infiltrates ("ischemic WMD"). Furthermore, low doses of LPS that by themselves have no adverse effects in 7-day-old rats (maturation corresponding to the near term human fetus), dramatically increase brain injury to a subsequent hypoxic-ischemic challenge, implicating that bacterial products can sensitize the immature CNS. Contrary to this finding, other bacterial agents like lipoteichoic acid were recently shown to induce tolerance of the immature brain suggesting that the innate immune system may respond differently to various ligands, which needs to be further explored. MRDD Research Reviews 2002;8:30,38. © 2002 Wiley-Liss, Inc. [source] Diffusion Tensor and Functional Magnetic Resonance Imaging of Diffuse Axonal Injury and Resulting Language ImpairmentJOURNAL OF NEUROIMAGING, Issue 4 2007Hui Mao PhD ABSTRACT Diffuse axonal injury (DAI) is a common aftermath of brain trauma. The diagnosis of DAI is often difficult using conventional magnetic resonance imaging (MRI). We report a diffusion tensor imaging (DTI) study of a patient who sustained DAI presenting with language impairment. Fractional anisotropy (FA) and DTI tractography revealed a reduction of white matter integrity in the left frontal and medial temporal areas. White matter damage identified by DTI was correlated with the patient's language impairment as assessed by functional MRI (fMRI) and a neuropsychological exam. The findings demonstrate the utility of DTI for identifying white matter changes secondary to traumatic brain injury (TBI). [source] Pestivirus as a cause of white matter damage -down but not outDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 4 2006Janet Rennie No abstract is available for this article. [source] Absence of pestivirus antigen in brains with white matter damageDEVELOPMENTAL MEDICINE & CHILD NEUROLOGY, Issue 4 2006Olaf Dammann We previously suggested that antenatal pestivirus infection might play a role in the pathogenesis of perinatal brain white matter damage (WMD) in preterm infants. We have now examined 22 brains from stillborns and deceased newborns (both preterm and term) for the presence of bovine virus diarrhoea virus (BVDV) antigen. The brains of five females and five males with WMD (median gestational age 36.5wks), and nine female and three male controls (median gestational age 36.5wks) were used in the study. No BVDV antigen was detected in any of the 22 brains. We conclude that brain infection with BVDV is unlikely to play a role in WMD pathogenesis among preterm or term newborns. Further research is needed to test the hypothesis that intrauterine exposure to pestivirus antigen elicits a fetal inflammatory response which then contributes to WMD. [source] Spontaneous kicking in full-term and preterm infants with and without white matter disorderDEVELOPMENTAL PSYCHOBIOLOGY, Issue 6 2010Linda Fetters Abstract Early damage to white matter of the brain may have developmental consequences for prematurely born infants including the coordination of leg movements. Our perspective is that white matter damage initiates an ontogenetic course that may lead to movement dysfunction leading to disability. In this study, spontaneous kicking in the human infant is a "window" for evaluating the potential consequences of perinatal brain damage for sensori-motor coordination. We compare the intra-limb coordination patterns of 5-month-old premature infants with white matter damage (PTWMD) to a group of prematurely born infants without WMD (PT) and a group of full-term (FT) infants. The PT group demonstrates advanced kicking patterns in comparison to both the PTWMD and FT groups. The PTWMD group has less mature patterns than the FT group on some, but not all measures. The movement challenge for PTWMD infants may be in the transition from spontaneous kicking to movements with the legs that require decoupling of intralimb joints. © 2010 Wiley Periodicals, Inc. Dev Psychobiol 52: 524,536, 2010. [source] Chronic effects of low to moderate alcohol consumption on structural and functional properties of the brain: beneficial or not?,HUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 3 2009Marinus N. Verbaten Abstract Objective Some studies suggest that the effects of low to moderate drinking (about 1,3 standard glasses of alcohol per day) on the brain and cognitive performance are positive. In the present study this hypothesis is investigated. Methods For this purpose studies on the effects of low to moderate drinking on brain structure (Magnetic Resonance Induction (MRI) studies) and on cognitive performance were analysed and discussed Results In MRI studies, a linear negative effect of alcohol consumption on brain volume was found. Furthermore, a linear decrease in grey matter concurring with a linear increase in white matter volumes as a function of number of drinks was reported in males, but not in females. Only in elderly low to moderate drinkers (aged,>,65 years) there appeared to be an U-shaped relationship between alcohol consumption and white matter integrity (grade) on the one hand and cognition on the other hand. Conclusions The changes reported in brain shrinkage, grey matter and white matter volume, as a result of low to moderate alcohol consumption sooner offer support for the contention that such drinking decreases brain health than for its beneficial effect. An exception might hold for elderly light and moderate drinkers where less white matter damage was found than in abstainers concurring with better cognitive performance. However, methodological problems impose limits on this conclusion. Copyright © 2009 John Wiley & Sons, Ltd. [source] Hypoxic damage to the periventricular white matter in neonatal brain: role of vascular endothelial growth factor, nitric oxide and excitotoxicityJOURNAL OF NEUROCHEMISTRY, Issue 4 2006Charanjit Kaur Abstract The present study examined factors that may be involved in the development of hypoxic periventricular white matter damage in the neonatal brain. Wistar rats (1-day old) were subjected to hypoxia and the periventricular white matter (corpus callosum) was examined for the mRNA and protein expression of hypoxia-inducible factor-1, (HIF-1,), endothelial, neuronal and inducible nitric oxide synthase (eNOS, nNOS and iNOS), vascular endothelial growth factor (VEGF) and N-methyl-D-aspartate receptor subunit 1 (NMDAR1) between 3 h and 14 days after hypoxic exposure by real-time RT-PCR, western blotting and immunohistochemistry. Up-regulated mRNA and protein expression of HIF-1,, VEGF, NMDAR1, eNOS, nNOS and iNOS in corpus callosum was observed in response to hypoxia. NMDAR1 and iNOS expression was found in the activated microglial cells, whereas VEGF was localized to astrocytes. An enzyme immunoassay showed that the VEGF concentration in corpus callosum was significantly higher up to 7 days after hypoxic exposure. NO levels, measured by colorimetric assay, were also significantly higher in hypoxic rats up to 14 days after hypoxic exposure as compared with the controls. A large number of axons undergoing degeneration were observed between 3 h and 7 days after the hypoxic exposure at electron-microscopic level. Our findings point towards the involvement of excitotoxicity, VEGF and NO in periventricular white matter damage in response to hypoxia. [source] Transient versus prolonged hyperlocomotion following lateral fluid percussion injury in mongolian gerbilsJOURNAL OF NEUROSCIENCE RESEARCH, Issue 2 2006Shihong Li Abstract Posttraumatic hyperactivity is a neurobehavioral symptom commonly seen in patients after traumatic brain injury (TBI). No useful animal model has yet been established for evaluation of this important symptom. We induced either mild (MILD, 0.7,0.9 atm) or moderate (MOD, 1.3,1.6 atm) lateral fluid percussion injury (LFPI) in Mongolian gerbils. Open-field and T-maze tests were used during a 7-day period after the trauma. All animals were perfusion fixed for histopathological examinations. Transient locomotor hyperactivity was found with a peak at 6 hr after injury in the MILD animals, whereas MOD animals showed prolonged and severe hyperlocomotion throughout the 7-day posttrauma period (P < 0.0001). Interestingly, the temporal profile of the posttraumatic hyperactivity was similar to that of the working memory deficit in both injury groups. Histological examination revealed significant neural tissue damages, including cortical necrosis, white matter rarefaction, and neuronal loss in the hippocampus in the ipsilateral hemisphere of the MOD animals, vs. only negligible changes in the MILD animals. Correlation analysis revealed that the volume of white matter lesions was significantly correlated with both posttraumatic hyperactivity (r = 0.591, P < 0.01) and working memory deficit (r = ,0.859, P < 0.0001). Taken together, our findings confirm the successful reproduction of posttraumatic hyperactivity following experimental TBI. The posttraumatic hyperlocomotion probably shared pathomechanisms common to those of cognitive dysfunction caused by LFPI, supporting the speculation from previous studies that some neurobehavioral abnormities intimately correlate with TBI-induced cognitive dysfunction. Histopathologically, significant involvement of white matter damage in the posttraumatic functional deficits was indicated. © 2006 Wiley-Liss, Inc. [source] Erythropoietin attenuates white matter damage, proinflammatory cytokine and chemokine induction in developing rat brain after intra-uterine infectionNEUROPATHOLOGY, Issue 5 2009Ying Shen To investigate the possible ameliorating effect of recombinant human erythropoietin (rhEPO) on white matter damage, pro-inflammatory cytokine and chemokine induction in developing rat brain after intra-uterine Escherichia coli infection. E. coli was inoculated into uterine cervix of the time-pregnant rats and the control was injected with normal saline. Following maternal E. coli inoculation, the pups received a single intraperitoneal injection of rhEPO at a dose of 5000 IU/kg body weight immediately after birth. Immunohistochemical staining and Western blot analysis for 2,, 3,-cyclic nucleotide 3,-phosphodiesterase (CNPase), neurofilament (NF) and glial fibrillary acidic protein (GFAP) were performed to assess white matter damage in pup brains at post-natal day 1 (P1), P3 and P7. Pro-inflammatory cytokines and chemokines were detected by real-time quantitative RT-PCR at the mRNA levels to evaluate the inflammatory response in pup brains at P1, P3 and P7. A single dose of rhEPO treatment (5000 IU/kg body weight) attenuated white matter damage in developing rat brain after intra-uterine E. coli infection. The protein levels of CNPase and NF in pup brains at P7 significantly increased after post-natal rhEPO treatment as compared with the intra-uterine E. coli -treated group. Also, post-natal rhEPO injection markedly attenuated the intra-uterine E. coli infection-induced increases in GFAP protein expression and the mRNA levels of pro-inflammatory cytokines and chemokines. Post-natal EPO administration as a single dose may exert a neuroprotective effect on white matter damage by reducing pro-inflammatory cytokine and chemokine induction in developing rat brain after intra-uterine E. coli infection. [source] Hereditary cerebral hemorrhage with amyloidosis-Dutch typeNEUROPATHOLOGY, Issue 4 2005Marion Maat-Schieman The amyloid ,-protein (A,) E22Q mutation of the rare disorder hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D) causes severe cerebral amyloid angiopathy (CAA) with hemorrhagic strokes of mid-life onset and dementia. The mutation does not affect total A, production but may alter the A,1,42:A,1,40 ratio, and affect the proteolytic degradation of A, and its transport across the blood,brain barrier. A, E22Q aggregates faster into more stable amyloid-like fibrils than wild-type A,. Non-fibrillar A,(x-42) deposits precede the appearance of fibrils and the deposition of A,(x-40) in the vascular basement membrane. CAA severity tends to increase with age but may vary greatly among patients of comparable ages. Lumenal narrowing of affected blood vessels, leukoencephalopathy, CAA-associated vasculopathies, and perivascular astrocytosis, microgliosis, and neuritic degeneration complicate the development of HCHWA-D CAA. Parenchymal A, deposition is also enhanced in the HCHWA-D brain with non-fibrillar membrane-bound A,(x-42) deposits evolving into relatively fibrillar diffuse plaques variously associated with reactive astrocytes, activated microglia, and degenerating neurites. Plaque density tends ,to ,decrease ,with ,age. ,Neurofibrillary ,degeneration is absent or limited. HCHWA-D dementia is associated with CAA severity independently of Braak stage, age, and plaque density. Particularly, microaneurysms may contribute to the development of (small) hemorrhages/infarcts and the latter to cognitive decline in affected subjects. However, the relative importance of cerebral hemorrhages/infarcts, white matter damage and/or other CAA- or A,-related factors for cognitive deterioration in HCHWA-D remains to be determined. [source] Traumatic axonal injury: practical issues for diagnosis in medicolegal casesNEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 2 2000J. F. Geddes In the 25 years or so after the first clinicopathological descriptions of diffuse axonal injury (DAI), the criterion for diagnosing recent traumatic white matter damage was the identification of swollen axons (,bulbs') on routine or silver stains, in the appropriate clinical setting. In the last decade, however, experimental work has given us greater understanding of the cellular events initiated by trauma to axons, and this in turn has led to the adoption of immunocytochemical methods to detect markers of axonal damage in both routine and experimental work. These methods have shown that traumatic axonal injury (TAI) is much more common than previously realized, and that what was originally described as DAI occupies only the most severe end of a spectrum of diffuse trauma-induced brain injury. They have also revealed a whole field of previously unrecognized white matter pathology, in which axons are diffusely damaged by processes other than head injury; this in turn has led to some terminological confusion in the literature. Neuropathologists are often asked to assess head injuries in a forensic setting: the diagnostic challenge is to sort out whether the axonal damage detected in a brain is indeed traumatic, and if so, to decide what , if anything , can be inferred from it. The lack of correlation between well-documented histories and neuropathological findings means that in the interpretation of assault cases at least, a diagnosis of ,TAI' or ,DAI' is likely to be of limited use for medicolegal purposes [source] Bronchopulmonary dysplasia and brain white matter damage in the preterm infant: a complex relationshipPAEDIATRIC & PERINATAL EPIDEMIOLOGY, Issue 6 2009Luigi Gagliardi Summary We analysed the relationship between bronchopulmonary dysplasia (BPD) and brain white matter damage (WMD) in very preterm infants, adjusting for common risk factors and confounders. We studied a cohort of infants <32 weeks gestational age (GA) and <1500 g, admitted to 12 hospitals in Northern Italy in 1999,2002. The association between BPD and WMD was estimated by generalised estimating equations and conditional logistic models, adjusting for centre, GA, propensity score for prolonged ventilation and other potential confounders. Directed acyclic graphs (DAG) were used to depict the underlying causal structure and guide analysis. Of the 1209 infants reaching 36 weeks, 192 (15.8%) developed BPD (supplemental oxygen at 36 weeks) and 88 (7.3%) ultrasound-defined WMD (cystic periventricular leukomalacia). In crude analysis, BPD was a strong risk factor for WMD [odds ratio (OR) = 5.9]. With successive adjustments, the OR progressively decreased to 3.88 when adjusting for GA, to 2.72 adding perinatal risk factors, and further down to 2.16 [95% confidence interval 1.1, 3.9] when ventilation was also adjusted for. Postnatal factors did not change the OR. Significant risk factors for WMD, in addition to BPD, were a low GA, a lower Apgar score, a higher illness severity score, ventilation and early-onset sepsis, while antenatal steroids, being small for GA, and surfactant were associated with a reduced risk. In conclusion, our data suggest that BPD is associated with an increased risk of WMD; most of the effect is due to shared risk factors and causal pathways. DAGs helped clarify the complex confounding of this scenario. [source] Gestational Hypoxia Induces White Matter Damage in Neonatal Rats: A New Model of Periventricular LeukomalaciaBRAIN PATHOLOGY, Issue 1 2004Olivier Baud In the premature infant, periventricular leukomalacia, usually related to hypoxic-ischemic white matter damage, is the main cause of neurological impairment. We hypothesized that protracted prenatal hypoxia might induce white matter damage during the perinatal period. Pregnant Sparague-Dawley rats were placed in a chamber supplied with hypoxic gas (10% O2 -90% N2) from embryonic day 5(E5) to E20. Neonatal rat brains were investigated by histology, immunocytochemistry, western blotting, in situ hybridization, DNA fragmentation analysis, and in vivo magnetic resonance imaging (MRI). Body weight of pups subjected to prenatal hypoxia was 10 to 30% lower from p0 to P14 than in controls. Specific white matter cysts wear detected between p0 and p7 in pups subjected to prenatal hypoxia, in addition to abnormal extra-cellular matrix, increased lipid peroxidation, white matter cell death detected by TUNEL and increased activated macrophage counts in white matter. Subsequently, gliotic scars and delayed myelination primarily involving immature oligodendrocytes were seen In vivo MRI with T1, T2, and diffusion sequences disclosed similar findings immediately after birth, showing strong correlations with histological abnormalities. We speculate that protracted prenatal hypoxia in rat induces abnormalities. We speculate that protracted prenatal hypoxia in rat induces white matter damage occurring through local inflammatory response and oxidative stress linked to re-oxygenation during the perinatal period. [source] Cognitive impairment and white matter damage in hypertension: a pilot studyACTA NEUROLOGICA SCANDINAVICA, Issue 4 2009K. Hannesdottir Objectives,,, Hypertension has been associated with impaired cognition. Diffusion tensor imaging (DTI) and magnetic resonance spectroscopy were applied to assess white matter abnormalities in treated vs untreated hypertension and if these correlated with neuropsychological performance. Methods,,, Subjects were 40 patients with medically treated hypertension (mean age 69.3 years), 10 patients with untreated hypertension (mean age 57.6 years) and 30 normotensive controls (mean age 68.2 years). Hypertension was defined as a previous diagnosis and taking hypertensive medication, or a resting blood pressure of >140/90 mmHg on the day of assessment. Results,,, Patients with treated hypertension performed worse on immediate (P = 0.037) as well as delayed memory tasks (P = 0.024) compared with normotensive controls. Cognitive performance was worse in untreated compared with treated hypertension on executive functions (P = 0.041) and psychomotor speed (P = 0.003). There was no significant correlation between cognition and any of the imaging parameters in treated hypertension. However, in untreated hypertension the results revealed a positive correlation between an executive functioning and attention composite score and DTI mean diffusivity values (P = 0.016) and between psychomotor speed and spectroscopy NAA/tCr levels (P = 0.015). Conclusions,,, These results suggest there is cognitive impairment in hypertension. Treated hypertension was associated with deficits in memory while untreated hypertension revealed a more ,subcortical' pattern of cognitive impairment. [source] Visual fields and optic disc morphology in very low birthweight adolescents examined with magnetic resonance imaging of the brainACTA OPHTHALMOLOGICA, Issue 8 2009Kerstin Hellgren Abstract. Purpose:, We aimed to evaluate visual fields (VFs) and optic disc morphology in very low birthweight (VLBW) adolescents compared with age- and gender-matched controls, and to relate the findings to magnetic resonance imaging (MRI) results. Methods:, Fifty-nine VLBW adolescents and 55 age- and gender-matched controls with normal birthweight were examined. Visual fields were tested using computerized rarebit perimetry (RB). Optic nerve and retinal vessel morphology were evaluated by digital image analysis of fundus photographs. Brain MRI was conducted in the VLBW subjects. Results:, Ten of the 57 VLBW subjects (p = 0.022) had subnormal VF results defined as a mean hit rate below the fifth percentile of the controls (i.e. < 89%). All of these also had significantly lower mean hit rates (p = 0.039) in the inferior hemifield. Sixteen of 57 (28%) VLBW subjects had white matter damage of immaturity (WMDI) on MRI. Six of 15 subjects with WMDI (who underwent VF testing) also had subnormal RB results, compared with four of 39 with normal MRI findings (p = 0.02). The mean neural retinal rim area was 9% smaller (p = 0.018) in the VLBW group than in the control group. The VLBW adolescents had a significantly higher index for tortuosity of arterioles than the controls (p < 0.001). Conclusions:, In the present study, 18% of all VLBW adolescents and 40% of those with WMDI had subnormal RB VF findings. The VLBW group had increased arterial tortuosity and a somewhat smaller (9%) mean neural retinal rim area than the control group. Thus sequels to VLBW appear to persist in adolescence. [source] Sonographic detection of the optic radiationACTA PAEDIATRICA, Issue 10 2005Annemieke Boxma Abstract Objective: To describe a region of hyperechoic white matter adjacent to the atrium of the lateral ventricle of preterms, and to speculate on the relevance of detecting preterm white matter injury. Patients and methods: Cranial ultrasound images of 92 preterms of gestational age (GA) 32 wk or less were reviewed. For each infant, one first week standard coronal image was used for measurement of grey values around the para-atrial region of interest (PAROI) relative to the choroid plexus. For verification of the sonographic anatomy, MR images of an adult brain were used. For reference, neuro-anatomical images were compared in several atlases. In a group of nine preterms of similar GA with cystic periventricular leukomalacia (PVL) or MR-confirmed white matter disease, the disappearance of the PAROI was examined. Results: The hyperechoic para-atrial area, subjectively detected in 84% of the patients, was situated bilaterally between the inner end of the lateral fissure and the upper third of the choroid plexus. In white matter caudal to the atrium, the hyperechoic band could be pursued towards the calcarine area. The average ratio of grey value around the PAROI to the choroid plexus was 0.787 (SD=0.072, median 0.791). There was no correlation between PAROI grey value and gestational age. At 26 wk gestational age, the average ratio was 0.781 (n=14), and 0.789 (n=17) at 31 wk. Location of the PAROI agrees with the angle of the upper loop of the optic radiation. None of the nine infants with white matter damage had PAROIs clearly distinguishable from flaring. Conclusion: The symmetrical and unchanged acoustic character between 26 and 31 wk of gestational age argues in favour of the hypothesis that the PAROI is an anatomical structure. The localization of the hyperechoic band supports the hypothesis that it represents part of the optic radiation. Further study is needed to examine the absence of a hyperechoic para-atrial band as a prognostic marker of the extension and severity of white matter injury. [source] Effect of maternal antibiotic treatment on fetal periventricular white matter cell death in a rabbit intrauterine infection modelACTA PAEDIATRICA, Issue 1 2003T Debillon Aim: To evaluate the effects of maternal antibiotic treatment on fetal brain cell death in a rabbit intrauterine infection model. Methods: After Escherichia coli uterine-horn inoculation in 22 pregnant rabbits, followed at various times by ceftriaxone and caesarean section, cell death in white matter (histology and fragmented DNA staining) from fetuses killed at extraction was compared across groups using the Mantel-Haenszel test and Fisher's exact test for small numbers. Results: White matter cell death was consistently present at 48 h, with ceftriaxone initiation at 24 h (group 1), detectable at 84 but not 60 h, with ceftriaxone initiation at 12 h, and significantly reduced at 84 h with ceftriaxone initiation at 6 h (60% vs 100% in group 1, p < 0.001, Fisher's exact test). Conclusion: Early maternal antibiotic therapy delays white matter cell death in rabbit fetuses exposed to intrauterine infection. This may provide a window for preventing white matter damage. [source] | ||||||||||||||||||||||||||||