Search

Background and Purpose: Brain growth in the early postnatal period following preterm birth has not been well described. This study of infants born at <30 weeks' gestational age and without major brain injury aimed to accomplish the following: 1) assess the reproducibility of linear measures made from cranial ultrasonography, 2) evaluate brain growth using sequential cranial ultrasonography linear measures from birth to term-equivalent age, and 3) explore perinatal predictors of postnatal brain growth., Materials and Methods: Participants comprised 144 infants born at <30 weeks' gestational age at a single center between January 2011 and December 2013. Infants with major brain injury seen on cranial ultrasonography or congenital or chromosomal abnormalities were excluded. Brain tissue and fluid spaces were measured from cranial ultrasonography performed as part of routine clinical care. Brain growth was assessed in 3 time intervals: <7, 7-27, and >27 days' postnatal age. Data were analyzed using intraclass correlation coefficients and mixed-effects regression., Results: A total of 429 scans were assessed for 144 infants. Several linear measures showed excellent reproducibility. All measures of brain tissue increased with postnatal age, except for the biparietal diameter, which decreased within the first postnatal week and increased thereafter. Gestational age of ≥28 weeks at birth was associated with slower growth of the biparietal diameter and ventricular width compared with gestational age of <28 weeks. Postnatal corticosteroid administration was associated with slower growth of the corpus callosum length, transcerebellar diameter, and vermis height. Sepsis and necrotizing enterocolitis were associated with slower growth of the transcerebellar diameter., Conclusions: Postnatal brain growth in infants born at <30 weeks' gestational age can be evaluated using sequential linear measures made from routine cranial ultrasonography and is associated with perinatal predictors of long-term development., (© 2018 by American Journal of Neuroradiology.)

Background: Few cUS studies of cerebral measurements are available for normal term infants. Normative data is important for evaluating cerebral structure size in symptomatic term infants and assessing preterm brain growth by term age., Objectives: To (i) make linear measurements using cranial ultrasound (cUS) for major cerebral structures and intracranial spaces in normal newborn term infants, (ii) correlate these measurements with gestational age (GA), birth weight (BW), head circumference (HC), gender and within one infant (iii) examine inter/intra-observer variation, and (iv) compare these data with those currently available., Design, Setting and Patients: Linear cUS measurements of major cerebral structures were made in well term-born Ugandan infants at Mulago University Hospital, Kampala. Correlations between the measurements and gender, HC, BW and GA were calculated. Intra- and inter-observer agreements were assessed., Results: Data from 106 infants (mean GA 39.20±1.4SD weeks) were analysed. Intra/inter-observer agreement was substantial/excellent. Significant correlations were found between HC and pons anterior-posterior diameter (p<0.01), corpus callosal (CC) length (p=0.02) and transverse cerebellar diameter (TCD, p<0.01) and between BW and CC length (p=0.02), vermis height (<0.01) and thalamo-occipital distance (p=0.03); no significant correlation was found with GA. Within infants CC length and TCD correlated significantly (p=0.019). Males had larger left ventricular indices than females (p=0.04). The data was similar to those from other populations., Conclusions: These data provide reliable reference values for linear measurements of many cerebral structures made using cUS. The data agree well with those from other populations suggesting that cerebral size is similar in different ethnic groups., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Background: There has been no study assessing cranial ultrasound (cUS) scans in newborn infants born in equatorial Africa., Objective: To assess the cUS scans of apparently well newborn term Ugandan infants and to correlate the findings with perinatal data., Methods: An observational study of apparently healthy postnatal ward term Ugandan infants at Mulago Hospital, Makerere University Hospital, Kampala, Uganda., Results: Data from 112 infants scanned at a median age of 1.4 postnatal days were analysed. Only 57 (51%) infants had scans considered normal, including 30 infants with isolated focal peritrigonal white matter (WM) echogenicity that was very common, occurring in 60 (53%) of infants. More extensive WM echogencities were seen in nine (7.5%) and focal unilateral central grey matter echogenicity in eight (6.5%) infants. Haemorrhage was not common. Subependymal pseudocysts (SEP) and choroid plexus cysts (CPC) occurred in 19.6% of infants each. Four infants only had lenticulostriate vasculopathy. No correlation was found between mode of delivery, birth weight, head circumference or gestational age, maternal HIV status and any cUS abnormality., Conclusions: Apparently well term-born Ugandan infants frequently have abnormalities on cUS. These are mainly increased WM echogenicity, SEP and CPC. These may relate to the reported high incidence of congenital infections in this population but this remains to be confirmed. The observations provide baseline data for comparison with scans from sick infants from similar communities and are also important for studies in which cUS will be used to assess progress.

Background and Purpose: Diffusion-weighted MR imaging studies of the adult brain have shown that contrast between lesions and normal tissue is increased at high b-values. We designed a prospective study to test the hypothesis that diffusion tensor imaging (DTI) obtained at high b-values increases image contrast and lesion conspicuity in the neonatal brain., Materials and Methods: We studied 17 neonates, median (range) age of 10 (2-96) days, who were undergoing MR imaging for clinical indications. DTI was performed on a Philips 3T Intera system with b-values of 350, 700, 1500, and 3000 s/mm(2). Image contrast and lesion conspicuity at each b-value were visually assessed. In addition, regions of interest were positioned in the central white matter at the level of the centrum semiovale, frontal and occipital white matter, splenium of the corpus callosum, posterior limb of the internal capsule, and the thalamus. Apparent diffusion coefficient (ADC) and fractional anisotropy (FA) values for these regions were calculated., Results: Isotropic diffusion image contrast and lesion-to-normal-tissue contrast increased with increasing b-value. ADC values decreased with increasing b-value in all regions studied; however, there was no change in FA with increasing b-value., Conclusions: Diffusion image contrast increased at high b-values may be useful in identifying lesions in the neonatal brain.

Background and Purpose: Brain imaging is an integral part of the diagnostic work-up for metabolic disorders, and the bedside availability of cranial ultrasonography (cUS) allows very early brain imaging in symptomatic neonates. Our aim was to investigate the role and range of abnormalities seen on cUS in neonates presenting with metabolic disorders. A secondary aim, when possible, was to address the question of whether brain MR imaging is more informative by comparing cUS to MR imaging findings., Materials and Methods: Neonates with a metabolic disorder who had at least 1 cUS scan were eligible. cUS images were reviewed for anatomic and maturation features, cysts, calcium, and other abnormalities. When an MR imaging scan had been obtained, both sets of images were compared., Results: Fifty-five infants (35 also had MR imaging) were studied. The most frequent findings were in oxidative phosphorylation disorders (21 cUS and 12 MR imaging): ventricular dilation (11 cUS and 6 MR imaging), germinolytic cysts (GLCs; 7 cUS and 5 MR imaging), and abnormal white matter (7 cUS and 6 MR imaging); in peroxisomal biogenesis disorders (13 cUS and 9 MR imaging): GLCs (10 cUS and 6 MR imaging), ventricular dilation (10 cUS and 5 MR imaging), abnormal cortical folding (8 cUS and 7 MR imaging), and lenticulostriate vasculopathy (8 cUS); in amino acid metabolism and urea cycle disorders (14 cUS and 11 MR imaging): abnormal cortical folding (9 cUS and 4 MR imaging), abnormal white matter (8 cUS and 8 MR imaging), and hypoplasia of the corpus callosum (7 cUS and 6 MR imaging); in organic acid disorders (4 cUS and 2 MR imaging): periventricular white matter echogenicity (2 cUS and 1 MR imaging); and in other disorders (3 cUS and 1 MR imaging): ventricular dilation (2 cUS and 1 MR imaging). cUS findings were consistent with MR imaging findings. cUS was better for visualizing GLCs and calcification. MR imaging was more sensitive for subtle tissue signal intensity changes in the white matter and abnormality in areas difficult to visualize with cUS, though abnormalities of cortical folding suggestive of polymicrogyria were seen on cUS., Conclusion: A wide range of abnormalities is seen using cUS in neonatal metabolic disorders. cUS is a reliable bedside tool for early detection of cysts, calcium, structural brain abnormalities, and white matter echogenicity, all suggestive of metabolic disorders.

Aicardi-Goutières syndrome is a rare progressive encephalopathy characterized by acquired microcephaly, basal ganglia calcification, and chronic CSF lymphocytosis, raised levels of interferon alpha in CSF and plasma and chill-blain type lesions. A possible mechanism of injury is cytokine related microangiopathy. We report brain imaging and proton (1H) and phosphorus-31 (31P) magnetic resonance spectroscopy (MRS) findings during the first year after birth in two patients. In patient 1 the evolution of brain metabolite ratios and intracellular pH obtained from serial 1H (long TE) and 31P MRS studies are described; in patient 2 a single 1H (short TE) MRS study is described. Imaging findings included basal ganglia calcifications, cerebral atrophy, and leukodystrophy. The MRS results demonstrated that Aicardi-Goutières syndrome is associated with reduced NAA/Cr, reflecting decreased neuronal/axonal density or viability, increased myo-inositol/Cr, reflecting gliosis or osmotic stress and a persisting brain lactic alkalosis. A brain lactic alkalosis has also been observed in those infants surviving perinatal hypoxia-ischaemia but with a poor neurodevelopmental outcome. A possible mechanism leading to brain alkalosis is up-regulation of the Na+/H+ transporter by focal areas of ischaemia related to the microangiopathy or by pro-inflammatory cytokines. Such brain alkalosis may be detrimental to cell survival and may increase glycolytic rate in astrocytes leading to an increased production of lactate.

Our aim was to assess brain myo-inositol/creatine plus phosphocreatine (Cr) in the first week in term infants with neonatal encephalopathy using localized short echo time proton magnetic resonance spectroscopy and to relate this to measures of brain injury, specifically lactate/Cr in the first week, basal ganglia changes on magnetic resonance imaging (MRI), and neurodevelopmental outcome at 1 y. Fourteen term infants with neonatal encephalopathy of gestational age (mean +/- SD) 39.6 +/- 1.6 wk, birth weight 3270 +/- 490 g, underwent MRI and magnetic resonance spectroscopy at 3.5 +/- 2.1 d. Five infants were entered in a pilot study of treatment with moderate whole-body hypothermia for neonatal encephalopathy; two were being cooled at the time of the scan. T(1)- and T(2)-weighted transverse magnetic resonance images were graded as normal or abnormal according to the presence or absence of the normal signal intensity of the posterior limb of the internal capsule and signal intensity changes in the basal ganglia. Localized proton magnetic resonance spectroscopy data were obtained from an 8-cm(3) voxel in the basal ganglia using echo times of 40 and 270 ms, and the peak area ratios of myo-inositol/Cr and lactate/Cr were measured. Outcome was scored using Griffith's development scales and neurodevelopmental examination at 1 y. MRI and outcome were normal in six infants and abnormal in eight. myo-Inositol/Cr and lactate/Cr were higher in infants with abnormal MRI and outcome (p < 0.01, p < 0.01, respectively). myo-Inositol/Cr and lactate/Cr were correlated (p < 0.01) and were both correlated to the Griffith's developmental scales (p < 0.01, p < 0.01, respectively). In conclusion, these preliminary data suggest that early increases in brain basal ganglia myo-inositol/Cr in infants with neonatal encephalopathy are associated with increased lactate/Cr, MRI changes of severe injury, and a poor neurodevelopmental outcome at 1 y.

We have found that cerebral lactate can be detected later than 1 month of age after neonatal encephalopathy (NE) in infants with severe neurodevelopmental impairment at 1 y. Our hypothesis was that persisting lactate after NE is associated with alkalosis and a decreased cell phosphorylation potential. Forty-three infants with NE underwent proton and phosphorus-31 magnetic resonance spectroscopy at 0.2-56 wk postnatal age. Seventy-seven examinations were obtained: 25 aged <2 wk, 16 aged > or = 2 to < or = 4 wk, 25 aged > 4 to < or = 30 wk, and 11 aged > 30 wk. Neurodevelopmental outcome was assessed at 1 y of age: 17 infants had a normal outcome and 26 infants had an abnormal outcome. Using univariate linear regression, we determined that increased lactate/creatine plus phosphocreatine (Cr) was associated with an alkaline intracellular pH (pHi) (p < 0.001) and increased inorganic phosphate/phosphocreatine (Pi/PCr) (p < 0.001). This relationship was significant, irrespective of outcome group or age at time of study. Between outcome groups, there were significant differences for lactate/Cr measured at < 2 wk (p = 0.005) and > 4 to < or = 30 wk (p = 0.01); Pi/PCr measured at < 2 wk (p < 0.001); pHi measured at < 2 wk (p < 0.001), > or = 2 to < or = 4 wk (p = 0.02) and > 4 to < or = 30 wk (p = 0.03); and for N-acetylaspartate/Cr measured at > or = 2 to < or = 4 wk (p = 0.03) and > 4 to < or = 30 wk (p = 0.01). Possible mechanisms leading to this persisting cerebral lactic alkalosis are a prolonged change in redox state within neuronal cells, the presence of phagocytic cells, the proliferation of glial cells, or altered buffering mechanisms. These findings may have implications for therapeutic intervention.

Background and Purpose: MR imaging of the brain can be used to detect cerebral damage after suspected hypoxic-ischemic injury. This study examines the reproducibility and accuracy of MR imaging soon after severe birth asphyxia., Methods: During a 48-month period, full-term newborn neonates, who died within the first week as a result of severe hypoxic ischemic encephalopathy, were included in the study if they had undergone early (<5 days old) MR imaging and postmortem neuropathologic studies. Two trained observers assessed reproducibility by examining multiple brain regions independently with current criteria and then defining and applying improved criteria. Accuracy of MR findings was tested by comparing the brain regions about which the two imaging raters agreed to those regions about which the two pathologists agreed., Results: Eight neonates, with a median gestational age of 40 weeks (range, 38-40 weeks) and who suffered severe birth asphyxia, were included in the study. In the reproducibility study, MR imaging agreement was moderate when current criteria were used (k = .44). Using the improved criteria, agreement increased considerably (k = .62). Much of this improvement was due to limiting the analyses to the posterior limb of the internal capsule, thalamus, parietal cortex, hippocampus, and medulla. The posterior limb of the internal capsule was the most reliable region analyzed. MR imaging agreement was similar to that achieved by two experienced pathologists reviewing the histologic sections (k = .66). In the accuracy study, MR imaging abnormality was predictive of pathologic abnormality with a sensitivity of .79 and a positive predictive value of 1.0. The predictive value of a single MR imaging abnormality was .79 (95% confidence interval, .61-.96)., Conclusion: Criteria that provide substantial reproducibility and accuracy for the interpretation of MR imaging findings very early after birth asphyxia can be derived.

In this prospective study proton magnetic resonance spectroscopy (1H MRS) was used to test the hypothesis that lactate can be detected later than 1 mo after birth in the brains of infants who display severe neurodevelopmental impairment 1 y after transient perinatal hypoxia-ischemia. Data were obtained from three groups of infants: 1) eight infants suffering birth asphyxia followed by perinatal encephalopathy and abnormal neurodevelopmental outcome at 1 y of age (defined as major neurologic impairment, Griffiths quotient <85%, and low optimality score); 2) 10 infants with signs of perinatal hypoxia-ischemia but normal neurodevelopmental outcome at 1 y; and 3) six control infants with uneventful perinatal courses and normal neurodevelopment at 1 y. Between one and four examinations (median 1) were performed at median (range) 11 (4-68) wk after birth, and the cerebral concentration ratio of lactate to creatine plus phosphocreatine (Cr) calculated from each spectrum. Lactate was detected later than the 1st mo after birth in seven of eight infants with abnormal neurodevelopmental outcome [maximum detected lactate/Cr was median (range) 0.44 (0.24-0.67)]. No lactate was detected later than the 1st mo after birth in infants with normal neurodevelopmental outcome, nor in five of six control subjects, although a small amount of lactate was detected in one control infant (lactate/Cr=0.04). These results suggest that the pathologic postasphyxial process, indicated by persistent cerebral lactate, may not be confined to the period immediately after injury.

Objective: The aim of this study was to establish whether abnormal signal intensity in the posterior limb of the internal capsule (PLIC) on magnetic resonance imaging is an accurate predictor of neurodevelopmental outcome at 1 year of age in infants with hypoxic-ischemic encephalopathy (HIE)., Methods: We have examined 73 term neonates with HIE between 1 and 17 days after birth with cranial magnetic resonance imaging and related the magnetic resonance imaging findings to neurodevelopmental outcome at 1 year of age., Results: All infants with an abnormal signal intensity in the PLIC developed neurodevelopmental impairment although in 4 infants with very early scans the abnormal signal was not apparent until up to 4 days after birth. A normal signal intensity was associated with a normal outcome in all but 4 cases; 3 of these infants had minor impairments and all had persistent imaging changes within the white matter. The 4th infant with a normal signal intensity on day 2 died before a further image could be obtained. The absence of normal signal predicted abnormal outcome in term infants with HIE with a sensitivity of 0.90, a specificity of 1.0, a positive predictive value of 1.0, and a negative predictive value of 0.87. The test correctly predicted outcome in 93% of infants with grade II HIE, according to the Sarnat system. Applying a Bayesian approach, the predictive probability of the test (the probability that the test would predict an outcome correctly) was distributed with a mean of 0.94 and 95% confidence limits of 0.89 to 1.0., Conclusion: Abnormal signal intensity in the PLIC is an accurate predictor of neurodevelopmental outcome in term infants suffering HIE.

Advances in magnetic resonance technology have revolutionized our ability to obtain detailed images of the neonatal brain without the use of ionizing radiation. Magnetic resonance imaging has now become the modality of choice for the in-vivo assessment of brain development, myelination and pathology.

Purpose: To compare conventional two-dimensional multisection images with registered three-dimensional volume and subtraction images for detecting subtle changes in the brains of infants and children., Methods: Twenty-six patients (24 with hemorrhagic/ischemic lesions) and one each with perinatal infection and Sturge-Weber disease were examined on two or more occasions with conventional multisection T1- and T2-weighted sequences as well as with 3-D T1-weighted volume sequences. A registration program was used to match the volume images to subvoxel dimensions, and subtracted images (second volume set minus the first) were obtained. The multisection images were compared with the 3-D and subtracted images and graded for detection of changes in a variety of brain structures., Results: In 16% to 33% of comparisons of different structures, the multisection images and the 3-D registered and subtracted images showed changes equally well. The 3-D registered and subtracted images were better than the multisection images in 67% to 84% of comparisons for detection of changes in the cerebral hemispheres, ventricles, brain stem, cerebellum, and in lesions. Statistically significant differences were found between the graded performance of the registered 3-D images and the conventional 2-D images in detecting cerebral infarction and hypoxic ischemic encephalopathy. In the late phase following neonatal cerebral infarction (1 to 11 months), the 3-D registered and subtracted images revealed growth of the brain at the margins of the lesions., Conclusion: Subvoxel registration of serial MR images may be of value in detecting subtle changes in the brains of infants and children.

Proton magnetic resonance spectroscopy (1H MRS) was performed within 18 h of birth (median 13, range 4-18 h) on 16 term infants with clinical features of birth asphyxia. Ten infants with no evidence of birth asphyxia were studied as controls at 5-18 (median 8) h after birth. To detect delayed impairments in cerebral energy metabolism, 15 infants suspected of asphyxia underwent 31P MRS at 33-106 (median 62) h of age. Choline, creatine, and N-acetylaspartate (NAA) were detected in spectra located to the basal ganglia in all infants. Lactate was detected in 15 of the 16 infants suspected of asphyxia, but in only 4 of the 10 controls (p < 0.05, chi 2). Glutamine and glutamate (Glx) was detected in 11 infants suspected of asphyxia and in three controls, but this difference was not significant at the 5% level. The spectra revealed no other significant differences between asphyxiated infants and controls. In the asphyxiated infants, there was a negative correlation between the ratio of lactate to creatine in the first 18 h of life and phosphocreatine/inorganic phosphate (PCr/ P(i)) at 33-106 h (p < 0.001). Five severely asphyxiated infants had PCr/P(i) < 0.75 (median 0.53, range 0.14-0.65), indicating a poor neurodevelopmental prognosis, and a further infant died before PCr/Pi could be measured. Ten infants had PCr/P(i) > 0.75 (1.03, 0.76-1.49). Median lactate/creatine was 1.47 (range 0.67-3.81) in the six severely affected subjects, 0.38 (0-1.51) in the latter group, and 0 (0-0.6) in controls (p < 0.0005, Kruskall-Wallis). These results suggest that, after birth asphyxia, cerebral energy metabolism is abnormal during the period when 31P MRS characteristically gives normal results. 1H MRS might be of value in predicting which infants are likely to suffer a decline in cerebral high energy phosphate concentrations and subsequent neurodevelopmental impairment.

T2-weighted spin echo scans were performed on a neonate and two adults aged 42 and 60 years within 2 weeks of the onset of infarction in the frontoparietal region of the brain. Areas of increased signal intensity were observed in the anterior and posterior limbs of the internal capsule in the infant and in the posterior limbs of the internal capsules in the adults. Although these signal changes were typical of the chronic phase of Wallerian degeneration, their onset was much earlier than the 10-14 weeks previously described for this stage in adults. The low level of myelination of white matter tracts at birth, and the relatively sparse myelination of the parietopontine tract may account for the rapid onset of changes in these patients which more closely follows the time course described pathologically for Wallerian degeneration in unmyelinated fibres.

The contributions of CSF signal reduction, use of a long echo time and diffusion weighting to the appearance of pulsed gradient spin echo (PGSE) images are analysed by reference to T2-weighted spin echo and T2-weighted fluid attenuated inversion recovery (FLAIR) pulse sequences. Both PGSE and T2-weighted FLAIR sequences reduce CSF signal and produce very heavy T2 weighting allowing the specific additional contribution produced by the diffusion weighting of PGSE sequences to be recognized. Considerable advantage accrues from CSF suppression with both PGSE and FLAIR sequences through reduction in partial volume effects and artefacts. The very heavy T2 weighting with both these pulse sequences highlights certain white matter tracts and provides high sensitivity to disease. The additional diffusion weighting with PGSE sequences can enhance or reduce white matter tract signals and may enhance or reduce lesion conspicuity relative to the FLAIR sequences. Many of the benefits attributed to the diffusion-weighted PGSE sequence may result from the reduction of the CSF signal and the heavy T2 weighting of the sequence without a contribution from diffusion effects. However, additional anatomical detail, sensitivity to myelination and increased lesion conspicuity may result from the diffusion weighting.

Inversion recovery (IR) sequences with an inversion time (TI) designed to markedly reduce or null the signal from CSF (TI of approximately 2,100 ms at 1.0 T) and a very long echo time (TE) of 240 ms were used to image the brain of two normal adult volunteers, one 34-year-old man with an intrinsic tumor, and one 3-month-old infant with an infarct. Using these very heavily T2-weighted pulse sequences, adult gray and white matter showed similar signal intensity in many areas of the brain, but normal white matter in regions of the centrum semiovale, posterior internal capsule, parietopontile tract, occipitothalamic radiation, and brain stem showed a much higher signal intensity than surrounding gray or white matter. The infant displayed a low signal intensity in myelinated regions in the internal capsule and occipitothalamic radiation and a high signal in unmyelinated white matter. In many of the images there were strong similarities to the distribution of high signal within white matter seen with pulsed gradient spin echo sequences (TE 130 ms) designed to demonstrate effects due to anisotropic diffusion. Arguments are advanced to support the view that the high signal intensity in white matter tracts is due to one or more long T2 components that may be associated with unmyelinated or sparsely myelinated fibres within white matter. The resemblance to diffusion weighted images may reflect the fact that both employ long TEs and both produce a low signal from CSF. If myelin possessed a different susceptibility from axoplasm so that magnetic field gradients were generated around nerve fibres when their orientation was not parallel to B0, diffusion of water might then produce the observed dependence on fibre direction. The high signal regions in white matter are a potential source of confusion in image interpretation, and measurements of T2 in white matter need to be made with these regional variations in mind. The concept of normal appearing white matter also needs to be applied with a knowledge of these differences. The IR sequences used in this study provide a very high T2 dependence with a low signal from CSF and may be useful for detecting disease in the CNS of adults and children.

Brain MR examinations were performed on one normal and 30 abnormal neonates and infants with a variety of clinical problems using pulsed gradient spin echo (PGSE) sequences sensitized in different directions to detect changes due to anisotropically restricted diffusion of water within the brain. Anisotropically restricted diffusion was demonstrated within white matter, which appeared to be myelinated with T1-weighted inversion recovery or spin echo sequences and within white matter where the presence of myelin was not demonstrated with these sequences. Cysts and fluid collections were recognised by their low signal intensity using PGSE sequences in the subcortical regions, lentiform nuclei, and periventricular regions. An intracerebral hematoma and a subdural hematoma showed a high signal intensity with PGSE sequences consistent with isotropically restricted diffusion. Chronic infarction displayed a low signal intensity consistent with relatively free isotropic diffusion. Patients with leukodystrophy associated with congenital muscular dystrophy showed an anisotropic pattern with different components of the abnormality present on images with sensitization in different directions. The corticospinal tracts failed to show highlighting in three cases where conventional imaging was normal. In several patients with a history of birth asphyxia, asymmetry and a relative reduction in signal intensity were seen in the corticospinal tracts.

Proton magnetic resonance spectroscopy (MRS) was used to study the brain of 2 normal and 15 abnormal infants aged from 33 weeks postmenstrual age (PMA) to 14 months postnatal age. Eleven of the infants were examined on at least two occasions. The principal clinical diagnoses in the abnormal infants were perinatal ischemic and hemorrhagic brain injury. All proton spectra demonstrated peaks that were assigned to N-acetylaspartate (NAA), choline containing compounds (Cho), and creatine plus phosphocreatine (Cr). The NAA/Cho and NAA/Cr ratios increased with age, while the Cho/Cr ratio decreased with age in the majority of infants. The NAA/Cho ratio was generally lower in abnormal infants, but the difference was not apparent before 40 weeks (PMA). This ratio was lowest in infants with the severest degree of neurological abnormality. Proton and phosphorus MRS was compared in seven infants. In those with severe brain lesions, early phosphorus spectra were abnormal. On follow-up the phosphorus spectra became normal, but the proton spectra showed persistently low NAA/Cho and NAA/Cr ratios. Proton MRS provides new information that may be complementary to phosphorus MRS in the diagnosis and monitoring of brain development in normal and neurologically damaged infants.

The purpose of this study was to evaluate the relation between cranial blood flow (CBF) and arterial blood pressure (BP) in the human newborn. In 29 healthy term neonates simultaneous measurements of CBF using jugular venous occlusion plethysmography and BP using the neonatal Dinamap 847 were performed during active sleep (AS) and quiet sleep (QS) at least 1 h from th end of the last feed. In AS as compared to QS there was significant rise in CBF (P less than 0.001), mean arterial (P less than 0.001), systolic (P less than 0.001), diastolic (P less than 0.005) and pulse pressure (P less than 0.027). There was a significant correlation between change in the mean arterial pressure (MAP) and change in CBF (r=0.37, P less than 0.05). No correlation, however, was found between changes in CBF and changes in systolic, diastolic or pulse pressures.