Neonatal Cerebral Investigation
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Skip to main content. Book Review Book Review. In an interestingly titled page book, Neonatal Cerebral Investigation , Drs Rennie, Hagmann, and Robertson have edited a multiauthored text 9 contributors, none of whom are radiologists , which covers 3 major areas: The physical principles of sonography US , the principles of electroencephalography EEG , and the basic principles of MR imaging and MR spectroscopy.
Previous Next. Back to top. In this issue. American Journal of Neuroradiology Vol. Table of Contents Index by author. Download PDF. Article Alerts. Email Article. Thank you for your interest in spreading the word on American Journal of Neuroradiology. You are going to email the following Neonatal Cerebral Investigation.
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Neonatal Cerebral Investigation - Janet M Rennie - Bok () | Bokus
Assisted Ventilation of the Neonate Jay P. Newborn Carole Arsenault. Engaging Infants Frances Thomson-Salo. Examination of the Newborn Anne Lomax. The S. Program: Learner Manual Kristine A. Nursing the Neonate Maggie Meeks. Table of contents Preface; Glossary and abbreviations; 1. Principles of ultrasound; 2.
Principles of EEG; 3. Principles of magnetic resonance imaging and spectroscopy; 4. Normal neonatal imaging appearances; 5. The immature brain; 7. The baby with a suspected seizure; 8.
Cerebral infarcts complicating neonatal leptomeningitis
The baby who was depressed at birth; 9. Screening the preterm infant at high risk of brain injury; Common maternal and neonatal conditions that may lead to neonatal brain imaging abnormalities; The baby and the fetus with abnormally large cerebral ventricles; Investigations of the baby with abnormal antenatal brain scan or suspected congenital malformation of the brain; Investigation of the baby with suspected CNS infection; Postmortem imaging; Index.
Review quote 'Neonatal Cerebral Investigation fulfils a key role in educating the neonatologist caring for any infant at high risk of such neurological complications More than two thirds of the textbook applies a clinically relevant approach based on the fundamentals of the technology and its application in normative development Highly recommended to neonatologists, pediatric neurologists and radiologists.
The imaging quality is superb and the figures are of the highest caliber. The diagnostic review of various problems often includes helpful tables and algorithms for the author's academic approach to these issues This book fills a very important void in the field of neonatology and does so with a superb presentation. There are many beautiful colour illustrations. An excellent glossary and list of abbreviations in the beginning of the book are most useful. About Janet M. Rennie Janet M. Cornelia F. Nicola J. Learn about new offers and get more deals by joining our newsletter. Sign up now.
Follow us. Christmas Posting Dates here. If this is the case, neonatal cerebral infarction may be responsible for some cases of hemiplegic cerebral palsy in babies reported to have completely unremarkable perinatal histories. It is sometimes assumed that hemiplegic signs in infancy, which may be associated with contralateral computed tomography changes, are likely to be antenatal in origin unless there is a clearly documented history of perinatal insults.
The computed tomograms in our cases showed acute changes rather than established atrophy, and the transient seizure disorders suggested an acute neurological event.
Cerebral infarction can therefore occur in the few days before or after birth in healthy infants without overt underlying pathology. This was not a prospective study, and the imaging and investigations were performed according to clinical need, rather than as part of a research protocol. Because the progress following initial discharge from hospital was usually benign, there was rarely an indication for a follow up computed tomogram.
Sequential changes on magnetic resonance imaging MRI following neonatal cerebral infarction have recently been closely documented by Mercuri et al. We are therefore open to the criticism that the original computed tomography findings may have been misinterpreted, the diagnosis of cerebral infarction erroneous, and the good prognosis therefore much less surprising.
However, all of our cases presented with clinical seizures, all the computed tomograms were reported by consultant neuroradiologists, and table 3 shows that there was ancillary evidence of a focal cerebral lesion in many cases. Our finding of a good medium term prognosis following presentation with seizures and a computed tomographic diagnosis of neonatal cerebral infarction is therefore clinically relevant, even considering the constraints of a retrospective review and lack of follow up imaging. Although periventricular and subcortical infarction may be visualised very well by cerebral ultrasonography, we found that scanning with 5 and 7.
Ultrasound imaging may be normal even when interpreted in the light of information from a computed tomogram fig 2. Others have suggested, like us, that ultrasonography has limitations in the diagnosis of neonatal cerebral infarction. Koelfen et al 13 found that all six infants with computed tomographic evidence of neonatal cerebral infarction had abnormal ultrasound scans, and Perlman et al 6 used ultrasonography as a primary investigation and only proceeded to MRI if ultrasound scanning suggested neonatal cerebral infarction.
Our data do not support this view.
The pathology of neonatal cerebral infarction is unknown, and few necropsy data are available because the babies rarely die. Some have suggested an embolic or thrombotic origin; these reports have been reviewed by Mannino and Trauner. Some infarctions clearly correspond to the vascular distribution of a major cerebral artery—usually the middle cerebral—but this is not always the case. We did not see the unexplained predominance of left sided lesions reported by other authors.
Most of the published reports of neonatal cerebral infarction concern very small numbers of patients. Lien et al 5 have looked at risk factors for early onset neonatal seizures of any cause, but there are no previous published data comparing perinatal risk factors for neonatal cerebral infarction with controls.
The case control data presented here concern a very small number of cases, and the analysis clearly has a very low power. As neonatal cerebral infarction is likely to have a multifactorial origin, it is not surprising that our study sheds very little light on possible aetiology.
In two cases endotracheal intubation was performed in the context of meconium stained liquor, and the umbilical cord artery pH was above 7. The postnatal course also suggests that the cases were not significantly asphyxiated as none had a low 5 minute Apgar score or a clinical course consistent with hypoxic-ischaemic encephalopathy. We used babies who had been admitted to the neonatal unit as controls because we wanted to compare haematological and biochemical results with cases.
We felt it would be inappropriate to include as controls infants who had been admitted to the unit because of concerns about prolonged resuscitation, metabolic acidosis, or clinical suspicion of hypoxic-ischaemic encephalopathy. Koelfen et al 13 have reported a small series with a high incidence of assisted delivery, but this was not seen in our study.
Fetal Haemodinamic and Neonatal Cerebral Circulation in Maternal Threatened Preterm Labor
We have no evidence of cocaine abuse in any of the mothers of our cases, and none of the 12 was a twin. Polycythaemia has been implicated as a cause of neonatal cerebral infarction. One baby with neonatal cerebral infarction had an initial haematocrit of 70 and received a dilutional exchange transfusion, but the rest all had an initial haematocrit of 60 or less. The very low incidence of hemiplegic cerebral palsy at follow up was surprising. The parents were counselled that unilateral motor deficit of some degree was the most likely outcome.
However, the previously published reports summarised in table 5 show a wide range of outcomes. Prognosis of neonatal cerebral infarction in term infants published data. However, our study shows significant motor deficit in one of 12 cases. One case was lost to follow up at 11 months but the rest were assessed at 20 months or more and judged to be normal, apart from one child with an obvious hemiparesis.
This study confirms previous suggestions that cognitive development is unlikely to be seriously impaired following neonatal cerebral infarction. All of our cases, including the child with hemiparesis, were thought to have normal cognitive and sensory development when last seen, although they were not formally tested. Wulfeck et al reported that half of their cases showed a degree of language delay, although there was no significant delay in global cognitive function.
We have established that 11 of 12 of these children are functioning without apparent disadvantage in the medium term, but problems may, of course, become apparent at school age. None has a persisting seizure disorder at present, although late recurrence of seizures after an eight year seizure free interval has been documented by Sran and Baumann.