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Biomedical subjects

P Govaert

Publications and source records attributed to P Govaert.

At least 19 recordsLinked to original sources
PubMed2006

Heart rate changes are insensitive for detecting postasphyxial seizures in neonates.

We studied heart rate (HR) changes during 169 seizures (mean 12 per patient, range 8 to 18) in 14 neonates with severe birth asphyxia. HR changes were found in 21 seizures (12.4%) in eight patients (HR increases in four, decreases in one, and both patterns in three patients), suggesting the existence of neonatal cerebral hemispheric connections with brainstem autonomic regulatory centers. HR monitoring appears to be insensitive for detecting postasphyxial neonatal seizures.

Arrhythmias, Cardiac↗
PubMed2006

White matter damage in neonatal enterovirus meningoencephalitis.

The authors report six neonates with enteroviral meningoencephalitis. Five infants presented with prolonged seizures, and one presented with systemic enteroviral disease. Cranial ultrasonography showed increased echogenicity in the periventricular white matter, and MRI confirmed mild to severe white matter damage in all infants, which looked similar to periventricular leukomalacia. Two infants developed cerebral palsy: one was neurologically suspect at age 18 months, and three were developmentally normal.

Brain↗
PubMed2004

Arterial infarction caused by carotid artery dissection in the neonate.

Arterial stroke in a neonate caused by carotid artery dissection is rare. We report two cases, one with dissection at the level of the skull base, one just distal to the carotid bulb. Non-invasive techniques like MR angiography and sonography demonstrated the dissection accurately. MR imaging, especially the diffusion-weighted images, showed the extension and site of the cerebral infarction. In one case dissection could be suspected following vacuum and forceps extraction. In the other no obvious birth trauma was reported. In conclusion, in a neonate with clinical signs suggestive of cerebral infarction, dissection of the carotid artery should be considered.

Carotid Artery, Internal, Dissection↗
PubMed2001

Neonatal infarction within basal cerebral vein territory.

In this report, an unusual intracranial haemorrhage in a term male infant born to a mother with diabetes is explained on the basis of occlusion of both basal veins of Rosenthal. This diagnosis relies on anatomical location and iconographic aspect of the clots. Evidence that this vessel is occluded cannot be ascertained from ultrasound or MR angiographic techniques in the neonatal period. The basal vein has not been implicated in previous reports of neonatal brain haemorrhage.

Adult↗
PubMed2000

Perinatal cortical infarction within middle cerebral artery trunks.

AIM: To define neonatal pial middle cerebral artery infarction. METHODS: A retrospective study was made of neonates in whom focal arterial infarction had been detected ultrasonographically. A detailed study was made of cortical middle cerebral artery infarction subtypes. RESULTS: Forty infarctions, with the exception of those in a posterior cerebral artery, were detected ultrasonographically over a period of 10 years. Most were confirmed by computed tomography or magnetic resonance imaging. Factor V Leiden heterozygosity was documented in three. The onset was probably antepartum in three, and associated with fetal distress before labour in one. There were 19 cases of cortical middle cerebral artery stroke. The truncal type (n=13) was more common than complete (n = 5) middle cerebral artery infarction. Of six infarcts in the anterior trunk, four were in term infants and five affected the right hemisphere. Clinical seizures were part of the anterior truncal presentation in three. One of these infants, with involvement of the primary motor area, developed a severe motor hemisyndrome. The Bayley Mental Developmental Index was above 80 in all of three infants tested with anterior truncal infarction. Of seven patients with posterior truncal infarction, six were at or near term. Six of these lesions were left sided. Clinical seizures were observed in three. A mild motor hemisyndrome developed in at least three of these infants due to involvement of parieto-temporal non-primary cortex. CONCLUSIONS: Inability to differentiate between truncal and complete middle cerebral artery stroke is one of the explanations for the reported different outcomes. Severe motor hemisyndrome can be predicted from neonatal ultrasonography on the basis of primary motor cortex involvement. Clinical seizures were recognised in less than half of the patients with truncal infarction; left sided presentation was present in the posterior, but not the anterior truncal type of infarction. Asphyxia is a rare cause of focal arterial infarction.

Asphyxia Neonatorum↗
PubMed2000

Congenital CMV-infection and hearing loss.

CMV (cytomegalovirus) is one of the Herpesviridae, known for their potential for latency and reactivation. The sequelae of fetal infection are diverse: chronic stage of early fetal infection with brain anomalies, symptomatic late fetal infection with hepatitis and thrombocytopenia and asymptomatic infection. With any of these clinical phenotypes, permanent hearing loss is possible. CMV-infection is the only relevant viral cause of perinatal hearing loss because rubella, measles and mumps have become rare due to vaccination. Recent studies have suggested beneficial effects on outcome of i.v. ganciclovir treatment in symptomatic cases. We have recently taken the challenge of treating asymptomatic newborns on the basis of active sonographic brain lesions in order to prevent labyrinth destruction. We would also like to stress the importance of suspecting children with congenital hearing loss, or hearing loss that develops in the first year of life, of having an asymptomatic congenital CMV-infection. Follow up in the first years of life is necessary in these children because further progression of hearing loss is possible.

Child↗
PubMed1999

Neonatal focal temporal lobe or atrial wall haemorrhagic infarction.

AIMS: To describe two variants of infarction within the temporal lobe, associated with local matrix bleeding and mild to moderate intraventricular haemorrhage. METHODS: The files of 10 neonates, extracted from a sonographic study of 560 very low birthweight infants conducted between 1993 and 1997, were retrospectively examined. RESULTS: Seven lesions were located in the middle to posterior area of the temporal lobe, three others faced the atrium. All except two of those with a temporal site were VLBW infants with hyaline membrane disease. Except for one fatal case, intraventricular bleeding was mild to moderate. Computed tomograms or magnetic resonance imaging were used to illustrate the haemorrhagic nature of three lesions. Survivors of this so far undescribed entity who were followed up for more than 18 months did not have a uniform type of cerebral palsy but some scored in the low normal range on the Bayley Mental Development Index. One girl developed temporal lobe epilepsy. CONCLUSIONS: This pattern of injury seems to be one of venous infarction associated with temporal or para-atrial matrix haemorrhage. The temporal site fits the picture of venous infarction within the area drained by the inferior ventricular vein. A less constant lateral atrial vein, either draining into the basal or internal cerebral vein, is probably involved in the para-atrial lesion. Sonography may be the only practical tool currently available for detection in life.

Brain Infarction↗
PubMed1998

Otological manifestations of CHARGE association.

The combined findings of abnormalities of the incus and stapes, absence of the oval window, absence of the stapedius muscle (with absent pyramidal eminence and tympanic sinus in most cases), and abnormalities of different parts of the inner ear (dysplastic cochlea, hypoplastic or dysplastic vestibule, and absent semicircular canals) are characteristic of the CHARGE association. Computed tomography and magnetic resonance imaging using 1-mm-thick contiguous slices proved useful in demonstrating the broad spectrum of temporal bone abnormalities in patients with the CHARGE association.

Adolescent↗
PubMed1997

Subependymal caudothalamic groove hyperechogenicity and neonatal chronic lung disease.

Chronic lung disease is associated with several poorly defined risk factors for impaired cerebral development. Late neonatal onset of subependymal hyperechogenic areas in the caudothalamic groove has been reported in association with dexamethasone treatment and postnatal cytomegalovirus infection. We reviewed charts of 18 patients who developed subependymal hyperechogenicity beyond the first week of life, as well as charts of 79 patients belonging to a prospective surfactant study group. Thirteen of the 18 patients with subependymal hyperdensities had been treated with surfactant and were all found in the subgroup with chronic lung disease. In the surfactant-treated patients who did not develop chronic lung disease, we could not find any patient with subependymal hyperdensities. From the remaining five patients with ultrasound lesions, but who were not treated with surfactant, three had developed chronic lung disease. There was no evident association with dexamethasone treatment or cytomegalovirus infection. Our results support the idea of an association between chronic lung disease and the described echographic lesions in the caudothalamic groove, but the nature of the link between them is still unclear.

Betamethasone↗
PubMed1996

Use of tissue type plasminogen activator in neonates: case reports and review of the literature.

Recombinant tissue type plasminogen activator (rt-PA) has been used successfully in neonates for resolution of thrombotic processes, both arterial and venous. We report on 2 neonates with vena cava inferior thrombosis and with biochemical evidence of liver dysfunction in whom rt-PA treatment had to be interrupted because of significant bleeding tendency, without complete resolution of the thrombus. Therapy failure may be due to the age of the thrombus and the systemic way of administration, bypassing the site of the thrombus by collateral circulation. Impaired liver function may result in decreased degradation of rt-PA with prolonged effect and higher risk for bleeding complications. We suggest that lower doses should be administered in these patients.

Hemorrhage↗
PubMed1995

Nature of the brain lesion in fetal allo-immune thrombocytopenia.

Study of three fetuses with allo-immune thrombocytopenia, one with autopsy findings, and comparison with existing data have permitted speculation on the nature of the initial lesion within the brain. The commonest first bleeding site is probably underneath the molecular layer of the cerebral cortex, often within the temporal lobe. Small haemorrhages may appear to be (sub)pial, but expansion will lead to so-called subarachnoid haematoma. Communication with the adjacent lateral ventricle will contribute to post-haemorrhagic hydrocephalus. Occasionally, the initial haemorrhage is within the ventricle; such a pattern may lead to post-haemorrhagic hydrocephalus, often with a porencephalic component. In utero follow-up of fetuses at risk for allo-immune thrombocytopenia will have to focus on superficial cerebral haemorrhage for early detection of brain involvement.

Brain↗
PubMed1995

Rapidly progressive enlargement of the fourth ventricle in the preterm infant with post-haemorrhagic ventricular dilatation.

Six preterm infants who developed disproportionate enlargement of the 4th ventricle during the neonatal period, associated with post-haemorrhagic ventricular dilatation (PHVD), before shunt placement are reported. Five of the six preterm infants developed cyanotic spells and/or bradycardias at the time of rapid enlargement of the 4th ventricle, suggestive of raised posterior fossa pressure, which resolved following insertion of and drainage from a subcutaneous reservoir. In one of the three survivors an isolated 4th ventricle was subsequently diagnosed later in infancy, requiring drainage. These data suggest that a combination of an enlarged 4th ventricle on ultrasound and cyanotic spells and/or bradycardias should lead to rapid release of raised pressure in the posterior fossa. Long-term follow-up of these children is necessary, as isolation of the 4th ventricle can subsequently develop.

Cerebral Hemorrhage↗
PubMed1994

Aminoterminal propeptide of type III procollagen in cord blood and amniotic fluid of high-risk pregnancies: a biochemical approach to the dynamic assessment of deviant fetal growth.

N-terminal propeptide of type III procollagen (PIIINP) concentration was measured in cord serum, amniotic fluid, and maternal serum from high-risk pregnancies. The fetal PIIINP variability was shown to be independent of the maternal serum PIIINP values. Although a highly significant negative correlation was found between the fetal propeptide level and gestational age in both appropriate-for-gestational-age neonates (n = 504) and small-for-gestational-age infants (n = 98), the PIIINP concentration in cord serum or amniotic fluid of small-for-gestational-age infants was significantly lower compared with that of appropriate-for-gestational-age infants matched for postconceptional age. PIIINP assay may thus serve as a dynamic biochemical indicator of deviant fetal growth. The PIIINP results were also related to the severity or duration of intrauterine growth retardation, as indicated by significantly lower propeptide cord serum values in nonmalformed small-for-gestational-age infants with small head circumference, known as an index for the chronicity of fetal nutritional deprivation. Preeclampsia, maternal diabetes or smoking, and congenital anomalies appeared not to be associated with any alteration of fetal propeptide concentration, provided they did not cause fetal growth deceleration. The finding of extremely high cord serum PIIINP values in six newborn infants with the Potter malformation sequence led to the speculation that large amounts of propeptides or their fragments usually are excreted by the fetal kidneys into the amniotic fluid. We suggest that determination of the PIIINP level in amniotic fluid or cord serum, obtained by amniocentesis and percutaneous umbilical sampling, may be a helpful adjunctive biochemical parameter in future research protocols assessing fetuses at risk for intrauterine growth retardation.

Amniotic Fluid↗
PubMed1992

Vacuum extraction, bone injury and neonatal subgaleal bleeding.

In a population of 27 flemish newborns with subgaleal bleeding encountered within a period of 6 years, we studied the obstetrical, clinical and radiological data. In contrast with controversial findings from the available literature, there is little doubt that difficult, often elective vacuum extraction is the main cause of this neonatal emergency. Disturbances in haemostasis, when documented, were attributed to focal intrahaematoma consumption, except for one boy who presented with haemophilia and neonatal subgaleal bleeding. Conventional X-ray examination continues to be of importance for the documentation of suture diastasis, fissures and fractures. CT scan reveals both the amount of extra-osseous bleeding, the degree of bone displacement and injury as well as the type and extent of associated intracranial damage. Subgaleal haemorrhage rarely hides a growing synchrondrosal rupture.

Birth Injuries↗
PubMed1992

Deep cerebral venous thrombosis in thalamo-ventricular hemorrhage of the term newborn.

Unilateral thalamic bleeding with associated intraventricular hemorrhage is reported in three full-term neonates. The first presented within 48 hours from birth with early onset streptococcal meningitis, persistent pulmonary hypertension, tonic seizures and a tense fontanelle. The second presented 6 days after birth with irritability, opisthotonus, a tense fontanelle and tonic seizures. The third was admitted three days after birth with seizures and a tense fontanelle. In the latter two infants NMR and CT imaging documented thrombosed superficial and deep cerebral veins. The etiopathogenesis of intracranial venous thrombosis in the neonate is diverse: asphyxia, dehydration, polycythemia, sepsis-meningitis and difficult delivery are the main causes. In one of our patients jugular vein compression by the collar of a negative-pressure ventilation chamber probably initiated the intracranial events. More than half of the survivors sustain severe neurological impairment.

Cerebral Hemorrhage↗