PubMed Health⌕ Search

Biomedical subjects

Maarten Lequin

Publications and source records attributed to Maarten Lequin.

7 recordsLinked to original sources
PubMed2006

Postnatal onset cortical dysplasia associated with infarction of white matter.

On MRI at 35 weeks of a boy born at 25 weeks, focal disorganization of the cortex was observed near a frontal venous infarct developed in the first week. Disruption of the final steps of cell migration, injury to the subplate and/or disruption of corticospinal axons are possible mechanisms behind it. Preterms with white matter lesions at or below 25 weeks postconceptional age should be scrutinized for cortical dysplasia.

Cerebral Cortex↗
PubMed2006

Sonographic templates of newborn perforator stroke.

BACKGROUND: Many paediatric strokes occur in the perinatal period. Improvement in neuroimaging has increased detection in newborns with neurological symptoms. OBJECTIVE: To define sonographic templates of neonatal stroke in the territory of perforators of the anterior choroidal artery (AChA) and the anterior (ACA), middle (MCA) and posterior (PCA) cerebral arteries. MATERIALS AND METHODS: In 24 neonates with perforator stroke, we retrospectively studied antenatal and perinatal events. Brain sonography was performed with an 8.5-MHz probe. Only hyperechoic lesions in the thalamus and/or striatum and/or centrum semiovale were included. MRI was obtained using a 1.5-T machine. RESULTS: We detected 28 perforator strokes in 24 infants (6 preterm): 5 MCA medial striate, 8 MCA lateral striate, 3 MCA centrum semiovale, 4 ACA Heubner's, 5 PCA thalamic arteries, 1 AChA, and 2 hypothalamic perforators. We attributed clinical seizures to stroke in two infants only. Catheter-related embolism (certain in three, possible in six others) and birth trauma (two) were probable causes. Specific conditions were found in six others. Only one infant (in nine evaluated) had an increased prothrombotic risk (fII mutation). In describing the lesions, we focused on the templates of infarction as seen in a parasagittal US sweep. Infarcts were confirmed by MRI in 21 patients. CONCLUSION: Our study showed that infarct topography can be evaluated reliably with brain sonography. This is important given the asymptomatic character of most lesions.

Brain↗
PubMed2006

Sonographic maturation of third-trimester cerebellar foliation after birth.

The development of cerebellar folia of third-trimester preterms has not been described with ultrasound before. We set out to determine normal development of the pons and cerebellar folia for future measurements of hypoplasia and atrophy. Study sonograms were made in preterms admitted to the neonatal intensive care unit with postmenstrual age (PMA) from 25 wk until term. On a weekly basis, transcranial measurements were made in the axial and coronal planes at the asterion with high-frequency transducers (8.5 and 13 MHz). The axial images showed the pons and fourth ventricle. The coronal images showed cerebellar folia and white matter. In the same coronal plane, the depth of cerebellar fissures at the rostral cerebellar convexity could be observed. A total of 172 cranial sonograms were performed on 98 neonates. The development of folia could be measured with ultrasound through the asterion. We showed that pons area, mean of three fissure depths, hemisphere area, and number of folia in the horizontal fissure correlated significantly with PMA. Hemisphere area described the same trend of growth as the transverse cerebellar diameter used in fetal sonography.

Cerebellum↗
PubMed2005

Sonographic detection of the optic radiation.

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.

Adult↗
PubMed2004

Sonographic appearance of the normal and abnormal insula of Reil.

Three planes are discerned during ultrasonographic screening of the insula in parasagittal view: opercular, insular, and fissural. Six newborn infants with normal brain anatomy, including two each of 28, 34, and 40 weeks' gestation, were selected for a description of the evolution of these parasagittal planes. Opercularization of the insula begins to be detected on a sonogram at about the 24th gestational week and progresses cranially. On coronal section the insular space forms a shallow groove at 24 weeks, becoming a slit at 28 weeks that grows longer and develops branches after 32 weeks. At 28 weeks the ascending anterior branch of the circular groove and the lateral fissure at the bottom of the insula are clearly seen in parasagittal section. Subsequent change consists of undulation and bifurcation of the lateral fissure, together with elongation of the anterior margin. Secondary gyri become visible in the insular dome between 28 and 34 weeks, forming short anterior and long posterior insular gyri. Five term newborn infants with perisylvian polymicrogyria were observed with both neonatal ultrasound and magnetic resonance imaging: two of unknown cause, and one each due to cytomegalovirus, bifunctional peroxisomal protein deficiency, and monozygous twinning. With polymicrogyria, on parasagittal sonographic examination at fissural level the anterior margin of the circular groove is a short rudiment. In insular view, only rudimentary sulci ascend from the lateral fissure; short and long gyri are not seen. In opercular view, no secondary branches are seen from the lateral fissure, an image akin to that seen at 28 weeks. A complete insular triangle is not recognized in any of these sections. A deep abnormal sulcus may prolong the lateral fissure when schizencephaly is associated with polymicrogyria. The insula in glutaric aciduria type II has no secondary gyri at term and is reduced to a simple and small triangle. Not all instances of polymicrogyria lead to macroscopically recognizable alteration of insular gyri.

Brain Diseases↗
PubMed2003

Changes in globus pallidus with (pre)term kernicterus.

OBJECTIVE: We report serial magnetic resonance (MR) and sonographic behavior of globus pallidus in 5 preterm and 3 term infants with kernicterus and describe the clinical context in very low birth weight preterm infants. On the basis of this information, we suggest means of diagnosis and prevention. METHODS: Charts and MR and ultrasound images of 5 preterm infants and 3 term infants with suspected bilirubin-associated brain damage were reviewed. Included were preterm infants with severe hearing loss, quadriplegic hypertonia, and abnormal hypersignal of globus pallidus on T2-weighted MR imaging (MRI). In 1 infant who died on day 150, the diagnosis was confirmed during the neonatal period. The others were picked up as outpatients and scanned at 12 or 22 months' corrected age. Three instances of term kernicterus were included for comparison of serial MRI in the neonatal period and early infancy: they were caused by glucose-6-phosphate dehydrogenase deficiency, urosepsis, and dehydration plus fructose 1-6 biphosphatase deficiency. RESULTS: Five preterm infants of 25 to 29 weeks' gestational age presented with total serum bilirubin (TSB) levels below exchange transfusion thresholds commonly advised. Mixed acidosis was present in 3 infants around the TSB peak. The bilirubin/albumin molar ratio was >0.5 in all, in the absence of displacing drugs. All failed to pass bedside hearing screen tests and had severe hearing loss on auditory brain response testing. Symmetrical homogeneous hyperechogenicity of globus pallidus was the alerting feature in 1 infant. Globus pallidus was hyperintense on T1-weighted MR images in this child. The other infants presented with severe developmental delay as a result of dyskinetic quadriplegia and hearing loss. Globus pallidus was normal on T1- but hyperintense on T2-weighted MR images at 12 or 22 months' corrected age. Subthalamic involvement was documented in coronal fluid attenuated inversion recovery MRI in 2 infants. The term infants with classical clinical presentation in the neonatal period had MR behavior similar to the preterms, but pallidal injury was not recognized with targeted sonographic examination. Their neonatal MR images demonstrated pallidal T1 hyperintensity and mild T2 hyperintensity. CONCLUSION: Acidotic very low birth weight preterm infants with low serum albumin levels develop MR-confirmed pallidal injury and hearing loss facing "accepted" TSB levels. Serial MRI documents a shift from acute mainly T1 hypersignal to permanent T2 hypersignal in globus pallidus within the late neonatal period. Subthalamic and not thalamic involvement helps to differentiate from ischemic or metabolic disorder. As newborns, these infants are rigid and have severe apnea, before developing hypertonic quadriplegia in infancy.

Echoencephalography↗