Occipital-frontal Head Circumference Research Articles

Microcephaly and Its Related Syndromes: Classification, Genetic, Clinical, and Rehabilitative Considerations

AbstractMicrocephaly, a form of cortical cortex malformation, results from abnormal cellular production and proliferation, identified when the occipital frontal head circumference (OFC) falls two or more standard deviations (SDs) below the expected average for age, gender, and population. Severity is classified based on SD: mild (OFC < 2 SD) or severe (OFC < 3 SD). While microcephaly can lead to developmental delay, intellectual disability, epilepsy, and cerebral palsy, not all cases exhibit these issues. Classified as primary/congenital or secondary/postnatal, microcephaly can stem from genetic or acquired factors in both types. Congenital microcephaly origins vary, while secondary microcephaly is characterized by normal OFC at birth, followed by a decrease within the first year, often associated with progressive cognitive and motor impairments. Primary hereditary microcephaly (MCPH), or microcephaly vera, is genetically diverse, with 28 related genes (MCPH1 to MCPH28) encoding proteins linked to centrosomes and progenitor cell mitosis in the brain ventricle's neuroepithelium. Defects in deoxyribonucleic acid (DNA) repair pathways (e.g., NBN, FANCA, ATR, ATM genes) can lead to microcephaly by impairing DNA repair. Enzyme deficiencies in metabolic pathways may also contribute, causing toxic metabolite accumulation or essential metabolite loss (microcephaly of metabolic origin). Acquired congenital microcephaly may result from ischemic or infectious processes, drugs, radiation, maternal diseases during pregnancy, with damage influenced by fetal genetics, environmental interactions, developmental stage, and exposure intensity/duration. Diagnostic workup includes electroencephalogram, ophthalmological, auditory, magnetic resonance imaging, metabolic, echocardiogram, and infection screening tests, alongside genetic evaluations like cytogenetic studies, fluorescence in situ hybridization, comparative genomic microarray-hybridization, single-nucleotide microarray-polymorphism, and exome sequencing. Symptomatic treatment is available, and genetic counseling is crucial for affected families.

The clinical and genotypic-phenotypic findings of mucopolysaccharidosis VI patients: an Iraqi single-study descriptive study.

Maroteaux-Lamy syndrome (mucopolysaccharidosis type VI; MPS VI) is a chronic illness that causes progressive enlargement, inflammation, or scarring of several tissues and organs until their collapse. In most cases, an infant with MPS VI shows no symptoms. The early signs and symptoms of MPS VI in children often develop in the first few months of life. MPS VI affects various systems in the body, including the skeletal, cardiac, and respiratory systems. The authors aim in our study to describe the clinical and genotypic-phenotypic findings of MPS VI patients in 'children Welfare Teaching Hospital, Medical City Complex.' The single-center study was conducted at the 'children Welfare Teaching Hospital, Medical City Complex' from November 2016 to May 2022. The research recruited 72 MPS VI patients from Iraq, all under 20. The authors investigated the sociodemographic characteristics, hematological lab results, gene-phenotype findings, and clinical features and evaluated the severity and progression of the MPS 6 disease. Seventy-two Iraqi MPS VI patients were involved in the study, and the average age of the study sample was 6.38±3.4 (0.3-19). The consanguinity rate was 94.4%. In the research, females comprised 56.9% of the patients, and the Z-scores for body mass index and occipital-frontal head circumference were -2.66 and 1.2. The fascial features at diagnosis, 'coarse facies' (90.3%), dysostosis multiplex (93%), short stature (94.4%), and recurrent respiratory infections (91.6%), were the most common clinical features among the enrolled patients. The most frequent mutation was (complementary DNA: c.753C>G, protein effect: p.(Tyr2*) or p.(Tyr251Term), and the codon cross-tabulation: premature stop codon, or homozygous stop nonsense mutation/exon N.3) (33/69 (47.82%)). Furthermore, a statistically significant correlation existed between lower weight and height readings and the progressed and severe stages of the MPS VI illness. As the first research in Iraq with a sufficient sample size of MPS VI patients, the investigation presented important clinical and gene-phenotype findings and revealed the necessity for enhancing the diagnosis of MPS VI, including the updated molecular analysis and monitoring the multisystem parameters, aberrant comorbidities, and the progression and severity.

A CAMK2B variant associated with tetralogy of Fallot, developmental delay, and growth retardation

CAMK2B encodes the beta-subunit of calcium/calmodulin-dependent protein kinase II (CAMKII), which is expressed mainly in the brain. Variants of CAMK2A and CAMK2B cause neurodevelopmental disorders, and CAMK2B alterations have been described in at least 14 patients with intellectual disability and developmental delay. Here, we describe a novel CAMK2B variant in a patient with tetralogy of Fallot (TOF), developmental delay, and growth retardation. The patient was a 2-year-old female. She was delivered at 36 weeks 6 days gestational age by caesarean section due to non-reassuring fetal status, with birth weight of 1680 g (−2.0 SD), birth length of 43.5 cm (−1.5 SD), and occipital-frontal head circumference (OFC) of 29.4 cm (−1.7 SD). Growth retardation, microcephaly, developmental delay, tetralogy of Fallot, and dysmorphic features were present. The patient controlled her head position at four months, rolled at six months, sat at 13 months, crawled at 18 months, and walked with support at 21 months. She began speaking words at 2 years old. Her dysmorphic features included a wide face, broad forehead, puffy eyelids, broad nasal base, broad and prominent philtrum, pointed chin, full cheeks, and prominent ears. A de novo missense CAMK2B variant (NM_172079.2:c.895A > G (p.Lys299Glu) NC_000007.14:g.44241708T > C (hg38)) was identified by proband exome sequencing and confirmed by Sanger sequencing. The variant was located at an autoregulatory segment and highly conserved among species. This patient displayed many of the physical features of CAMK2B-related neurodevelopmental disorder (NDD), but the TOF present in the current case is not a feature of patients with the NDD. Since a de novo CAMK2B (p.Leu443Val) variant has previously been found in a cohort of TOF, we conclude that CAMK2B variants may be associated with this specific cardiac defect.

Head Growth in Children With Perinatal Stroke

Source: Leong A, Floer A, Kirton A, et al. Head circumference trajectory in children with perinatal stroke [published online ahead of print March 8, 2021]. J Child Neurol. doi:10.1177/0883073821996103Investigators from Alberta Children’s Hospital, Calgary, Canada, conducted a retrospective cohort study to evaluate longitudinal head growth in children with perinatal stroke. Children with perinatal stroke were identified through a population-based research cohort of children with MRI-confirmed unilateral arterial perinatal stroke and who had follow-up of more than 12 months with the Pediatric Stroke Outcome Measure (PSOM), a validated measure of neurologic deficit and function. Participants included in this current study were ≤18 years old and had no other systemic conditions. Demographics were collected at the time of cohort enrollment.The primary predictor was occipital-frontal head circumference (OFC) as obtained from the medical record. OFC data at different ages from the same participant from birth to 18 years old were included. The primary outcome was neurologic deficit, as measured by the PSOM. The PSOM is scored on a 10-point scale, with higher scores representing worse deficits. Investigators generated sex-segregated OFC plots from birth to 18 years old using the 50th percentile OFC at every 2-week interval between birth and 6 months of age, 1-month intervals from 6 months to 2 years of age, and 6-month intervals from 2 to 18 years of age. Investigators also compared the 50th percentile OFC among participants at each interval to the 50th percentile OFC of healthy American children serving as controls using OFC data obtained from a separate database. Lastly, investigators assessed whether there were more participants with PSOM scores ≥1 who had OFCs at <50th percentile (vs ≥50th percentile).There were 315 OFC measurements from 102 participants with perinatal stroke included in analysis. Overall, 52% participants were male. There was a mean of 2.8 OFC measurements among female participants and 3.2 OFC measurements among male participants. Overall, 28% (N = 29) of participants had a PSOM score of 0.The OFC for female participants followed the OFC for female healthy controls until age 3 months, at which point the 50th percentile OFC for female participants became significantly smaller compared to healthy controls. This effect also was observed for male participants, but the divergence occurred later at 18 months. There were significantly more participants with an OFC <50th percentile (vs ≥50th percentile) who had PSOM scores ≥1 (87% vs 52%; P = 0.004).Investigators conclude that there is a deceleration in head growth in children with perinatal stroke and worse neurological outcomes among those with an OFC <50th percentile.Dr Candee has disclosed no financial relationship relevant to this commentary. This commentary does not contain a discussion of an unapproved/investigative use of a commercial product/device.Perinatal stroke is the most common cause of hemiplegic cerebral palsy, occurring in roughly 1/2,300 term births and 7/1,000 preterm births.1 It is most often the result of ischemic injury to brain tissue, which then leads to encephalomalacia, volume loss, and a decrease in OFC.2 Although acquired microcephaly has been shown to be associated with poor neurologic development across a variety of conditions, the current investigators are the first to look specifically at the impact of head growth (using OFC trajectory as a surrogate) on neurologic development in children with a history of perinatal stroke.3The results of the current study confirm the suspected hypothesis of the investigators, namely that head growth deceleration occurs in children with perinatal stroke, and that OFC <50th percentile is associated with a worse neurological outcome (as measured by PSOM). Interestingly, the timing of OFC divergence between the study population and healthy controls occurred much earlier for girls (eg, 3 months, vs 1 year for boys). The study findings are strengthened by the exclusion of “higher-risk” children with systemic conditions or other non-stroke neurologic diagnoses. They potentially are limited in that the collective data could be biased by over-representation of the more severely affected patients (who may have had more measurements).Perinatal stroke often goes unnoticed until 4-6 months of life, when motor asymmetry, early hand preference, or seizures become evident.1 While OFC is only a rough estimate of head size in a mobile infant and therefore highly subject to measurement error, it is an inexpensive, noninvasive tool that can enable primary care providers to detect perinatal stroke or its complications (eg, infantile spasms or cerebral palsy) sooner. OFC measurements also potentially could facilitate the connection of infants with earlier individualized support or therapeutic interventions for optimizing development.Head growth deceleration in children with perinatal stroke is associated with poor developmental outcome.Hats off to research with results that underscore the continued value of physical examination rather than newer health care technology.

Head circumference trajectory in children with perinatal stroke.

Background:Perinatal stroke is a leading cause of hemiparetic cerebral palsy and lifelong disability. Neurodevelopmental outcomes are difficult to predict and markers of long-term poor outcome continue to be investigated. Deceleration in growth of head circumference has been associated with worse developmental outcomes in neonatal brain injury. We hypothesized that perinatal stroke would result in decreased rates of head growth during childhood that would be associated with worse developmental outcomes.Methods:Patients with magnetic resonance imaging (MRI)–confirmed neonatal arterial ischemic stroke and arterial presumed perinatal ischemic stroke were identified from a population-based research cohort (Alberta Perinatal Stroke Project). Demographics and occipital-frontal circumference data were collected from medical records. Head growth was compared to typically developing control charts using a 2-tailed t test. The Fisher exact test was used to examine associations between Pediatric Stroke Outcome Measures (PSOM) scores and occipital-frontal head circumference.Results:Three hundred fifteen occipital-frontal head circumference measurements were collected from 102 patients (48 female, 54 male), over a median of 3.2 years (standard deviation = 5.18, range = 0-18.3). After 3 months for female patients and 1 year for male patients, occipital-frontal head circumference deviated and remained below normal growth trajectories (P < .05) with a large effect size (Cohen d >0.8). Poor outcome (PSOM ≥ 1) was associated with smaller occipital-frontal head circumference (P < .05).Conclusion:Head growth deceleration is observed in children with perinatal arterial ischemic stroke and is associated with poor outcome. Head circumference may be a tool to alert clinicians to the potential of abnormal neurologic outcome.

Saethre-Chotzen syndrome: long-term outcome of a syndrome-specific management protocol.

AimTo assess the long‐term outcomes of our management protocol for Saethre–Chotzen syndrome, which includes one‐stage fronto‐orbital advancement.MethodAll patients born with Saethre–Chotzen syndrome between January 1992 and March 2017 were included. Evaluated parameters included occipital frontal head circumference (OFC), fundoscopy, neuroimaging (ventricular size, tonsillar position, and the presence of collaterals/an abnormal transverse sinus), polysomnography, and ophthalmological outcomes. The relationship between papilledema and its associated risk factors was evaluated with Fisher’s exact test.ResultsThirty‐two patients (21 females, 11 males) were included. Median (SD) age at first surgery was 9.6 months (3.1mo) for patients who were primarily referred to our center (range: 3.6–13.0mo), the median (SD) age at last follow‐up was 13 years (5y 7mo; range: 3–25y). Seven patients had papilledema preoperatively, which recurred in two. Two patients had papilledema solely after first surgery. Second cranial vault expansion was indicated in 20%. Thirteen patients had an OFC deflection, indicating restricted skull growth, one patient had ventriculomegaly, and none developed hydrocephalus. Eleven patients had emissary veins, while the transverse sinus was aberrant unilaterally in 13 (hypoplastic n=10 and absent n=3). Four patients had mild tonsillar descent, one of which was a Chiari type I malformation. Four patients had obstructive sleep apnoea (two mild, one moderate, and one severe). An aberrant transverse sinus was associated with papilledema (p=0.01).InterpretationSingle one‐stage fronto‐orbital advancement was sufficient to prevent intracranial hypertension for 80% of our patients with Saethre–Chotzen syndrome. Follow‐up should focus on OFC deflection and venous anomalies.

S14-03 SESSION 14: FACIOCRANIOSYNOSTOSIS – PART III SAETHRE-CHOTZEN SYNDROME: LONG-TERM OUTCOME OF A SYNDROME-SPECIFIC TREATMENT PROTOCOL

Introduction: To assess the long-term outcomes of our standard treatment protocol for Saethre-Chotzen syndrome (SCS), which includes one-stage fronto-orbital advancement (FOA). Methods: We included all patients born with SCS between Jan 1992- March 2017, the diagnosis was genetically confirmed. Evaluated parameters included occipital frontal head circumference (OFC), fundoscopy, neuro-imaging (i.e. ventricular size, tonsillar position, and the presence of collaterals/a deviant transverse sinus), polysomnography and ophthalmologic outcomes. Factors influencing proportional differences between patients with or without papilledema and with one versus more surgical interventions were evaluated with Fishers exact test. Results: We included 33 patients. The median age at first surgery was 9.6 months for patients primarily referred to our center (N=31). Seven patients had papilledema pre-operatively, which recurred in 2. Two patients had papilledema solely after first surgery. Second cranial vault expansion was indicated in 6 patients treated according to our treatment protocol (19%). One patient had ventriculomegaly, none developed hydrocephalus. Ten patients had venous collaterals, the transverse sinus was aberrant unilaterally in 12 (hypoplastic N=10, absent N=2). Four patients had tonsillar herniation (TH), one had a CM-I malformation. Four patients had OSA (2 mild, 1 moderate, 1 severe). An aberrant transverse sinus was associated with the occurrence of papilledema (P =0.03). Conclusion: A one-stage FOA is sufficient treatment for 81% of the patients with SCS. The follow-up in these patients should focus on OFC deflection and venous anomalies.

Muenke syndrome: long-term outcome of a syndrome-specific treatment protocol.

The authors evaluated the long-term outcome of their treatment protocol for Muenke syndrome, which includes a single craniofacial procedure. This was a prospective observational cohort study of Muenke syndrome patients who underwent surgery for craniosynostosis within the first year of life. Symptoms and determinants of intracranial hypertension were evaluated by longitudinal monitoring of the presence of papilledema (fundoscopy), obstructive sleep apnea (OSA; with polysomnography), cerebellar tonsillar herniation (MRI studies), ventricular size (MRI and CT studies), and skull growth (occipital frontal head circumference [OFC]). Other evaluated factors included hearing, speech, and ophthalmological outcomes. The study included 38 patients; 36 patients underwent fronto-supraorbital advancement. The median age at last follow-up was 13.2 years (range 1.3-24.4 years). Three patients had papilledema, which was related to ophthalmological disorders in 2 patients. Three patients had mild OSA. Three patients had a Chiari I malformation, and tonsillar descent < 5 mm was present in 6 patients. Tonsillar position was unrelated to papilledema, ventricular size, or restricted skull growth. Ten patients had ventriculomegaly, and the OFC growth curve deflected in 3 patients. Twenty-two patients had hearing loss. Refraction anomalies were diagnosed in 14/15 patients measured at ≥ 8 years of age. Patients with Muenke syndrome treated with a single fronto-supraorbital advancement in their first year of life rarely develop signs of intracranial hypertension, in accordance with the very low prevalence of its causative factors (OSA, hydrocephalus, and restricted skull growth). This illustrates that there is no need for a routine second craniofacial procedure. Patient follow-up should focus on visual assessment and speech and hearing outcomes.

A prospective longitudinal study of postnatal dentoalveolar and palatal growth: The anatomical basis for CAD/CAM‐assisted production of cleft‐lip‐palate feeding plates

This study describes the dentoalveolar and palatal growth during the first months of life. Knowledge concerning this development is essential to avoid unwanted events such as mucosal ulcerations or restriction of growth when cleft-lip and palate (CLP) patients are treated. The results involve the generation of CAD/CAM CLP-feeding plates. Intraoral impressions from 32 healthy newborns were taken monthly for 5months, supplemented by measurements of body weight, length, and occipital-frontal head circumference. The casts were digitalized, and two observers manually selected defined anatomical landmarks on virtual 3-D models. The distances between these landmarks were evaluted. Statistical analysis included an inter-rater agreement analysis and the determination of growth. In total, 213 casts were analyzed, with 65 models excluded because of inaccuracies in impression-taking or cast production. Overall longitudinal growth was 20.3%, whereas transversal growth reached a maximum of 21.1%. Vertical growth was 32.4% at the tuberal level. On the basis of these results, a semiautomated series of feeding plates allowing for monthly expansion could be generated. The acquired data serve as a useful reference for other pediatric and orthofacial investigations and treatments. One such application is the automated, fully virtual manufacture of CLP-feeding plates based on only one impression-taking. Our data reveal when caution is needed to prevent ulceration. The series of plates generated can minimize the time-consuming impression-taking and the production of further plaster models. The method of measurement is suitable for documentary purposes. Clin. Anat. 30:846-854, 2017. © 2017 Wiley Periodicals, Inc.

Diminished growth and lower adiposity in hyperglycemic very low birth weight neonates at 4 months corrected age.

Characterize the relationship between neonatal hyperglycemia and growth and body composition at 4 months corrected age (CA) in very low birth weight (VLBW) preterm infants. A prospective study of VLBW appropriate-for-gestation infants (N=53). All blood glucose measurements in the first 14 days and nutritional intake and illness markers until discharge were recorded. Standard anthropometrics and body composition via air displacement plethysmography were measured near term CA and 4 months CA. Relationships between hyperglycemia and anthropometrics and body composition were examined using multivariate linear regression. Infants with >5 days of hyperglycemia were lighter (5345 vs 6455 g, P⩽0.001), shorter (57.9 vs 60.9 cm, P⩽0.01), had smaller occipital-frontal head circumference (39.4 vs 42.0 cm, P⩽0.05) and were leaner (percent body fat 15.0 vs 23.8, P⩽0.01) at 4 months CA than those who did not have hyperglycemia, including after correcting for nutritional and illness factors. Neonatal hyperglycemia in VLBW infants is associated with decreased body size and lower adiposity at 4 months CA independent of nutritional deficit, insulin use and illness. Downregulation of the growth hormone axis may be responsible. These changes may influence long-term growth and cognitive development.

Growth in the neonatal period after repeat courses of antenatal corticosteroids: data from the ACTORDS randomised trial

ObjectiveTo determine the effect of repeated antenatal corticosteroids on postnatal changes in weight, linear growth and head circumference.MethodsMothers who entered the repeated dose of antenatal steroids (ACTORDS) trial were randomised...

Birth weight discordance of twin pairs and their subsequent growth patterns

Background: Few studies have compared the growth of a twin with its co-twin and particularly in relation to birth weight discordance.Aim: The study investigated how the degree of birth weight discordance affected subsequent growth.Methods: Birth weight discordance of 762 twin pairs was determined. Subsequent weight, height and occipital-frontal head circumference (OFC) measurements were obtained between the ages of 2–9 years. Corresponding standard deviations scores (SDS) were analysed according to birth weight discordance, sex and zygosity. Weight status was taken into account by assigning twins into sub-groups according to whether they were the heavier twin at birth and remained heavier, became the lighter of the twin pair or had the same weight, for subsequent measurements.Results and conclusions: The degree of birth weight discordance had little effect on subsequent growth except in monozygotic (MZ) twins with >20% discordance. Severe low birth weight ( < 1.95 kg) is more significant in suppressing subsequent growth than the degree of discordance per se. A surprisingly high proportion of twins reversed their weight status when reviewed at an older age.

Mutation Analysis of the ASPM Gene in 18 Pakistani Families With Autosomal Recessive Primary Microcephaly

Autosomal recessive primary microcephaly (MCPH) is a rare neurological disorder, in which the patients exhibit reduced occipital frontal head circumference (>3 standard deviations) and mild-to-severe mental retardation. Autosomal recessive primary microcephaly is genetically heterogeneous and 7 loci have been reported to date. Mutations in ASPM (abnormal spindle-like, microcephaly associated) gene are the most common cause of autosomal recessive primary microcephaly in the majority of the reported families. In the current investigation, we have located and studied 21 families with autosomal recessive primary microcephaly. Genotyping using polymorphic microsatellite markers linked to 7 autosomal recessive primary microcephaly loci revealed linkage of 18 families to the MCPH5 locus. Sequence analysis of the ASPM gene in 18 linked families detected 2 novel nonsense mutations (c.2101C>T/p.Q701X; c.9492T>G/p.Y3164X) in 2 families and 2 novel deletion mutations (c.6686delGAAA/p.R2229TfsX9; c.77delG/p.G26AfsX41) in 2 other families. Three previously described mutations (c.3978G>A/p.W1326X; c.1260delTCAAGTC/p.S420SfsX32; c.9159delA/p.K3053NfsX4) were also detected in 11 families. These identified mutations extended the body of evidence implicating the ASPM gene in the pathogenesis of human hereditary primary microcephaly.

The Relative Contributions of Brain, Cerebrospinal Fluid-Filled Structures and Non-Neural Tissue Volumes to Occipital-Frontal Head Circumference in Subjects with Autism

An increased prevalence of macrocephaly defined by occipital-frontal circumference (OFC) is a consistent finding in autism. Several possible mechanisms have been proposed, the most compelling being early brain overgrowth. However, the proportion of non-neural tissues (NNT) that contribute to OFC has not been reported. Using quantitative magnetic resonance imaging (MRI) methods we analyzed the relationships between OFC and total brain (TBV), ventricular, surface cerebrospinal fluid (CSF)/meningeal, and NNT volumes in subjects with autism. Sixty male subjects (34 autistic; 26 controls) seven years of age and older were used in this study. Compared to other measures, NNT volume was most significantly related to OFC (r values > 0.8, p<or=0.001), though NNT volume did not differ between the groups. Ventricular volume was also uniformly related to OFC (r approximately 0.3, p> 0.06). In contrast, the OFC-TBV relationship was less robust in those with autism (r=0.25, p<or=0.09) and only significant in the controls (r=0.58, p<or=0.001). Conversely, subjects with autism had a more robust and significantly different relationship between subarachnoid CSF/meningeal volume than controls (r=0.53 and 0.24; p<or=0.001 and 0.12, respectively). Possible explanations for these findings are discussed in the context of potential OFC differences that may occur in accelerated early brain growth associated with autism.

New Postnatal Growth Grids for Very Low Birth Weight Infants

To generate contemporary postnatal growth curves for hospitalized very low birth weight infants. Retrospective survey. Tertiary intensive care nursery. All surviving singleton, appropriate-for-gestational age infants with birth weight < or = 1500 g, born January 1, 1987, to May 31, 1991, who did not develop necrotizing enterocolitis (N = 205). Macronutrient intakes and body weights were recorded daily, with crown-heel length and occipital-frontal head circumference recorded weekly up to 105 days of age or hospital discharge, whichever occurred first. Growth curves were generated for four birth weight ranges: 501 through 750, 751 through 1000, 1001 through 1250, and 1251 through 1500 g. Compared to previously published growth curves, the current infants regained birth weight more quickly and exhibited larger average daily weight gains. These differences were most apparent in infants of lowest birth weight. The "premature growth grid" constructed by Dancis et al more than 40 years ago may no longer be a useful standard of early postnatal growth for present-day very low birth weight, appropriate-for-gestational-age infants. The new weight curves are a more accurate reflection of current in-hospital growth trends, especially for infants weighing < or = 1000 g at birth.

The relationships of transcephalic impedance, head growth and caloric intake to outcome in preterm infants.

Twenty-two preterm infants with birth weights less than 1 400 g were measured weekly with transcephalic impedance and occipital-frontal head circumference. Mean caloric intake/kg/day was calculated weekly. All infants were assessed at one year of age with Bayley Mental and Motor Scales and neurological assessment. Univariate and multivariate analyses were performed indicating that transcephalic impedance was the most powerful of the three measures as a predictor of sequelae.