Cases reported "Asphyxia Neonatorum"

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1/36. Parasagittal cerebral injury: magnetic resonance findings.

    Parasagittal cerebral injury is a specific pathologic lesion that can be found in full-term newborn babies suffering from hypoxic-ischemic encephalopathy. It is defined by the presence of cortical and subcortical white-matter necrosis involving the parasagittal and superomedial areas of the cerebral convexities. We report on two patients who showed parasagittal cerebral injury on magnetic resonance imaging. In both cases antecedents of hypoxic-ischemic encephalopathy were noted. In one of the patients basal ganglia involvement was also detected by cranial magnetic resonance imaging. In the follow-up studies the presence of upper-limb pyramidal signs and dyspraxia were two of the more pronounced symptoms. We will discuss the usefulness of neuroimaging, especially magnetic resonance imaging with coronal views, in the diagnosis of the parasagittal cerebral injury.
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2/36. Cytochrome oxidase deficiency presenting as birth asphyxia.

    Hypoxic-ischaemic encephalopathy (HIE) was diagnosed in an infant with acidosis. At 7 weeks of age further investigations revealed abnormal neuroimaging (CT and MRI scans) and a raised plasma and CSF lactate. A skeletal-muscle biopsy at 2 months of age confirmed the diagnosis of cytochrome oxidase deficiency. The course of the patient's disorder has taken that of a static encephalopathy (cerebral palsy). Inborn disorders of the respiratory chain should be considered in the differential diagnosis of HIE.
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ranking = 0.125
keywords = cerebral
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3/36. Neonatal cerebral venous thrombosis coexisting with bilateral adrenal hemorrhage.

    We report a case of severe perinatal asphyxia with both cerebral venous thrombosis and adrenal hemorrhage who survived with severe sequela including multicystic encephalomalasia, acquired microcephaly and blindness. Hematological investigations showed normal levels of anticardiolipin antibodies, protein c and S levels and activity, antithrombin iii levels. factor v Leiden mutation was negative. The adrenal hemorrhage resolved within three months with glucocorticoid therapy, the cerebral venous thrombosis resolved within two months without treatment. The literature on neonatal cerebral venous thrombosis is also reviewed.
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ranking = 0.875
keywords = cerebral
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4/36. Multiple cystic and focal encephalomalacia in infancy and childhood with brain stem damage.

    Two cases are described in which damage to the brain stem was associated with extensive necrosis of the cerebral hemisphere. In the first case--a monochorionic twin--there was clear evidence that injury of an ischaemic or hypoxic type had occurred during fetal life and some evidence that an inadequate share of the placental circulation was an important aetiological factor. In the second case death occurred 4 yr after an asphyxial episode at birth. The lesions in the hemispheres and brain stem were extensive, although less than in the first example. The lesions are discussed in the context of our knowledge of the anatomy and physiology of the developing nervous system. Although they cannot as yet be fitted into the concepts of "critical periods" and "vulnerable periods" of development, this is perhaps because observations on human cases are scanty in comparison with the extensive animal studies which have been reported. The lesions are contrasted and compared with those seen in animals.
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ranking = 0.125
keywords = cerebral
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5/36. Neonatal hyperinsulinemic hypoglycemia. Two case reports.

    Neonatal hyperinsulinemic hypoglycemia must be suddenly and appropriately diagnosed and treated to prevent any further neurological dysfunction and damage. Therefore, we report two cases of our observation. Case 1: birth asphyxia, episodes of hypoglycemia after delivery, hyperinsulinism and reduced IGFBP1 blood concentration. Clinical and laboratory pictures resolved progressively after 8 days of life, perfusions were stopped and the neonate began to suck breast milk. Case 2: negative familial and perinatal history. On the 3rd day of life he developed cyanosis, hypotonia, tremors and hypoglycemia. He was discharged with a diagnosis of cerebral injury and neonatal hypoglycemia. At 1 year of life the child showed progressive and heavy neurological damage. The RMN of the brain showed: enlarged ventricles and liquor spaces around the brain, particularly in the frontal region. hyperinsulinism was diagnosed in our Clinic. He began pharmacological treatment with diazoxide that permitted euglycemia. The ammonium was normal and excluded glutamate dehydrogenase deficiency (mutation of GLUD1 gene); diazoxide responsivity excluded mutations of SUR1 and KIR6.3 genes. At 9 years of life he showed motor and language retardation. Newborns with perinatal history of asphyxia may develop transient hyperinsulinism with absent neurological consequences. Persistent hypoglycemic or epileptic-like episodes, in particular on waking up, after meals or during banal infections, must be studied to reveal hyperinsulinism.
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ranking = 0.13299150491136
keywords = cerebral, ventricle
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6/36. Tourette's syndrome and neonatal anoxia: further evidence of an organic etiology.

    Studies of Tourette's syndrome have indicated that the etiology may be either primary or secondary. Secondary Tourette's syndrome has been reported in association with numerous neurological conditions, but there have been no previous reports of Tourette's syndrome and its relationship to neonatal anoxia. This report presents the case of a 15-year-old boy with a history of Tourette's syndrome and neonatal anoxia and examines whether or not there is a connection between the two. To test the hypothesis that this is the first documented case of cerebral anoxia at birth followed by Tourette's, a review of the pertinent literature on secondary Tourette's syndrome is presented. Evidence of perinatal anoxia, subsequent Tourette's syndrome, a negative family history, as well as an examination of the statistical chances of anoxia and Tourette's syndrome co-existing and of all previous reports of acquired Tourette's syndrome tend to favor an organic perinatal insult as having caused the later development of Tourette's syndrome in the case of this adolescent.
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ranking = 0.125
keywords = cerebral
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7/36. Fetal trauma: brain imaging in four neonates.

    The purpose of this paper is to describe brain pathology in neonates after major traffic trauma in utero during the third trimester. Our patient cohort consisted of four neonates born by emergency cesarean section after car accident in the third trimester of pregnancy. The median gestational age ( n=4) was 36 weeks (range: 30-38). Immediate post-natal and follow-up brain imaging consisted of cranial ultrasound ( n=4), computed tomography (CT) ( n=1) and post-mortem magnetic resonance imaging (MRI) ( n=1). pathology findings were correlated with the imaging findings ( n=3). Cranial ultrasound demonstrated a huge subarachnoidal hemorrhage ( n=1), subdural hematoma ( n=1), brain edema with inversion of the diastolic flow ( n=1) and severe ischemic changes ( n=1). In one case, CT demonstrated the presence and extension of the subarachnoidal hemorrhage, a parietal fracture and a limited intraventricular hemorrhage. Cerebellar hemorrhage and a small cerebral frontal contusion were seen on post-mortem MRI in a child with a major subarachnoidal hemorrhage on ultrasound. None of these four children survived (three children died within 2 days and one child died after 1 month). Blunt abdominal trauma during pregnancy can cause fetal cranial injury. In our cases, skull fracture, intracranial hemorrhage and hypoxic-ischemic encephalopathy were encountered.
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ranking = 0.125
keywords = cerebral
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8/36. Burst suppression on amplitude-integrated electroencephalogram may be induced by midazolam: a report on three cases.

    Continuous amplitude-integrated electroencephalogram (aEEG) recording with a cerebral function monitor is a useful tool to evaluate prognoses following perinatal asphyxia in term infants. Drugs may change the pattern of the conventional EEG. This report presents three infants treated with midazolam for status epilepticus and repetitive seizures who proved resistant to other anticonvulsants (phenobarbitone, lidocaine). The infants developed burst suppression patterns on aEEG concurrent with high serum levels of midazolam (900-7093 microg l(-1)). Following discontinuation of midazolam treatment, serum levels normalized and background patterns returned to normal voltage traces. CONCLUSION: These findings indicated that midazolam can cause burst suppression on aEEG. Therefore, the prognostic value of aEEG is limited in case of high serum levels of midazolam. serum levels of midazolam should be measured in infants who have burst suppression patterns on aEEG during midazolam treatment.
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ranking = 0.125
keywords = cerebral
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9/36. Detection of wallerian degeneration in a newborn by diffusion magnetic resonance imaging (MRI).

    We present the case of an infant with hypoxic-ischemic encephalopathy in whom wallerian degeneration is demonstrated in white-matter fiber tracts by diffusion magnetic resonance imaging (MRI). MRI was undertaken on days 2 and 9 and then at 9 months of age. On day 2, conventional MRI was normal, but diffusion MRI showed bioccipital abnormalities. On day 9, diffusion MRI showed marked abnormalities in the deep white matter of the occipital regions (left > right), corpus callosum, left posterior limb of the internal capsule, and left cerebral peduncle. water apparent diffusion coefficient values showed a significant reduction in the left occipital white matter and corpus callosum between days 2 and 9 while demonstrating the expected pseudonormalization in cortical gray matter. Images at 9 months showed left occipital porencephaly and atrophy of the left cerebral peduncle, with the infant displaying right hemiplegia at 18 months of age. In this case, the time course of diffusion changes differed between white and gray matter, with diffusion MRI showing delayed wallerian degeneration of the cerebral white matter. This case characterizes this degeneration with clinical and follow-up MRI at 9 months of age.
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ranking = 0.375
keywords = cerebral
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10/36. Early continuous video-EEG in acute near-total intrauterine asphyxia.

    The evolution of electroencephalographic changes after acute hypoxic-ischemic injury is poorly understood, as a clear time of insult is often absent and continuous electroencephalographic monitoring in the first 3 days after such injury has not been previously reported. Infants who suffer sudden profound asphyxia, often termed "acute near-total intrauterine asphyxia", have evidence of damage to the deep gray matter. In these infants it is possible to time the onset and duration of cerebral ischemia. This report describes early continuous video-electroencephalography from 3 hours after birth in an infant with the characteristic clinical and radiologic features of acute near-total intrauterine asphyxia.
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ranking = 0.125
keywords = cerebral
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