PubMed · 10794870
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T R Nelson. 2000. Three-dimensional imaging.. https://doi.org/10.1016/s0301-5629(00)00159-9
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BACKGROUND AND PURPOSE: To our knowledge, the upper limits of the thickness of normal meninges on neurosonograms are not known. We therefore established a nomogram for sonographic measurements of the leptomeninges (pia-glial plate) and assessed its usefulness in neurosonographic examinations of children with bacterial meningitis. METHODS: The pia mater-cortical glia limitans complex on the surface of the brain and in the sulcus of a frontal gyrus was measured on neurosonograms in 100 infants without meningeal disease in order to establish a nomogram of the thickness of this pia-glial plate, referred to as the leptomeninx. Effects of prematurity, age, sex, and single-layer (surface) versus double-layer (sulcus) measurements were analyzed. Meningeal thicknesses derived from a retrospective analysis of the neurosonograms of 33 patients with purulent meningitis and a prospective study of 22 patients with bacterial meningitis were compared with the nomograms. Clinical outcomes of children with meningeal thickening were compared with those of affected children with normal meninges. RESULTS: The distribution of sulci measurements was significantly asymmetrical around the mean. Statistical data showed no influence of prematurity and sex, but showed surface measurements to be more consistent than sulcal measurements. Older chronological age was related to slightly larger sulci, but did not influence the surface measurements. In children with bacterial meningitis, the surface meninges were less frequently thickened than were the sulci. Sulcal enlargement occurred often in combination with echogenic deposits in the sub-arachnoid space. CONCLUSION: Leptomeninges are best measured on the surface of a gyrus rather than in a sulcus, as the normal thickness of the sulci shows much more variability. Clinical outcome of bacterial meningitis cannot be predicted by presence or absence of meningeal thickening as the only sonographic abnormality.
The incidence of periventricular leukomalacia (PVL) in risk neonates was evaluated among 300 risk neonates in a prospective ultrasound study at the Pediatric Clinic of the Medical Faculty, University of Rostock. Perinatal risk factors for the development of PVL and gestational age were taken into consideration. Maternal infections during pregnancy were found to be a risk factor for development of PVL. A severe hyaline membrane disease was more frequently diagnosed in highly immature preterm neonates with postnatal PVL. The percentage of highly immature preterm neonates with postnatal PVL and severe hyaline membrane disease was higher in vaginal-born risk neonates. A correlation between 1-minute Apgar scores < or = 3 and postnatal PVL was found in more mature preterm neonates.
OBJECTIVES: The objective of this study was to know the incidence of periventricular leukomalacia and persistent periventricular echodensities in neonates with a birth weight < 1,500 g and to correlate cranial ultrasound findings with the developmental outcome of these babies at 18 months of corrected age. PATIENTS AND METHODS: We performed a cohort study of 319 newborns weighing 1500 g or less who were admitted to the Neonatal Intensive Care Unit of "12 de Octubre" Hospital between July 1990 and April 1994. Scans were performed while they were hospitalized and 183 surviving infants were followed up to 18 months of corrected age. Relative risks (rr) and 95% confidence intervals (95% CI) were calculated for sequelae according to neonatal cranial ultrasound abnormalities. Ninety-six infants with normal scans were considered as the control group. Persistent periventricular echodensities were classified as mild, moderate or severe. RESULTS: The incidence of periventricular leukomalacia was 3% (10/319) and of persistent periventricular echodensites was 11.2% (36/319). The percentage of sequelae was 5% for control infants, 15.6% (rr = 3, CI 95% = 0.94-8.8) for persistent periventricular echodensities, independent of its severity, 50% (rr = 9.7, CI 95% = 2.6-35) for moderate persistent periventricular echodensities and 78% (rr = 15.6, CI 95% = 6-38) for periventricular leukomalacia. CONCLUSIONS: Periventricular leukomalacia multiplies the number of sequelae by 15. Persistent periventricular echodensities, independent of its severity, does not multiply the number of sequelae significantly. However, moderate persistent periventricular echodensities multiply the number of sequelae by 9.