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PubMed1997

Neurodevelopmental dysfunction among nonreferred children with idiopathic megalencephaly.

PURPOSE: To determine whether nonreferred children with idiopathic megalencephaly show evidence of specific neurodevelopmental dysfunction compared with sibling control subjects and age-matched control subjects. DESIGN: Cross-sectional, case-control study in a large, suburban pediatric practice. Subjects included 20 children between the ages of 6 and 15 years with a head circumference at greater than the 98th percentile, 19 siblings of these children with normalsize heads, and 16 age-matched control subjects. Standardized tests of language, academic achievement, visuomotor integration, motor function, and neurodevelopmental function were administered. RESULTS: Multivariate analysis, with control for age, showed a main effect for the presence of megalencephaly (F = 3.2; p < 0.05). Follow-up univariate analyses, with control for age, showed that children with megalencephaly had poorer performance on tasks of upper limb speed, visuomotor control, running speed, bilateral coordination, visuomotor integration, naming fluency, and minor neurologic indicators. CONCLUSION: The relationship between idiopathic megalencephaly and external hydrocephalus in infants is discussed. Results show that so-called "benign" idiopathic megalencephaly in nonreferred school-age children appears to be a clinical entity associated with subtle motor problems and neurodevelopmental dysfunction.

Achievement↗
PubMed2003

Neurodevelopmental status at eight years in children with dextro-transposition of the great arteries: the Boston Circulatory Arrest Trial.

OBJECTIVES: Our goal was to determine which of the two major methods of vital organ support used in infant cardiac surgery, total circulatory arrest and low-flow cardiopulmonary bypass, results in better neurodevelopmental outcomes at school age. METHODS: In a single-center trial, infants with dextrotransposition of the great arteries underwent the arterial switch operation after random assignment to either total circulatory arrest or low-flow cardiopulmonary bypass. Developmental, neurologic, and speech outcomes were assessed at 8 years of age in 155 of 160 eligible children (97%). RESULTS: Treatment groups did not differ in terms of most outcomes, including neurologic status, Full-Scale or Performance IQ score, academic achievement, memory, problem solving, and visual-motor integration. Children assigned to total circulatory arrest performed worse on tests of motor function including manual dexterity with the nondominant hand (P =.003), apraxia of speech (P =.01), visual-motor tracking (P =.01), and phonologic awareness (P =.003). Assignment to low-flow cardiopulmonary bypass was associated with a more impulsive response style on a continuous performance test of vigilance (P <.01) and worse behavior as rated by teachers (P =.05). Although mean scores on most outcomes were within normal limits, neurodevelopmental status in the cohort as a whole was below expectation in many respects, including academic achievement, fine motor function, visual-spatial skills, working memory, hypothesis generating and testing, sustained attention, and higher-order language skills. CONCLUSIONS: Use of total circulatory arrest to support vital organs during heart surgery in infancy is generally associated with greater functional deficits than is use of low-flow cardiopulmonary bypass, although both strategies are associated with increased risk of neurodevelopmental vulnerabilities.

Boston↗
PubMed2003

Apolipoprotein E genotype and neurodevelopmental sequelae of infant cardiac surgery.

BACKGROUND: There has been increasing recognition of adverse neurodevelopmental sequelae in some children after repair of congenital heart defects. Even among children with the same cardiac defect, significant interindividual variation exists in developmental outcome. Polymorphisms of apolipoprotein E have been identified as a risk factor for worse neurologic recovery after central nervous system injury. METHODS: A single-institution prospective study of patients <or=6 months of age undergoing cardiopulmonary bypass for repair of congenital heart defects was undertaken to evaluate the association between apolipoprotein E genotype and postoperative neurodevelopmental dysfunction. Developmental outcomes were evaluated at 1 year of age by using the Bayley Scales of Infant Development. RESULTS: One-year evaluation was performed in 244 patients. After adjustment for preoperative and postoperative covariates-including gestational age, age at operation, sex, race, socioeconomic status, cardiac defect, and use of deep hypothermic circulatory arrest-the apolipoprotein E epsilon2 allele was associated with a worse neurologic outcome as assessed by the Psychomotor Developmental Index of the Bayley Scales of Infant Development (P =.036). Patients with the apolipoprotein E epsilon2 allele had approximately a 7-point decrease in the Psychomotor Developmental Index. CONCLUSIONS: Apolipoprotein E epsilon2 allele carriers had significantly lower Psychomotor Development Index scores at 1 year of age after infant cardiac surgery. The effect was independent of ethnicity, socioeconomic status, cardiac defect, and use of deep hypothermic circulatory arrest. An effect of the apolipoprotein E epsilon4 allele was not detected. Genetic polymorphisms that decrease neuroresiliency and impair neuronal repair after central nervous system injury are important risk factors for neurodevelopmental dysfunction after infant cardiac surgery.

Alleles↗
PubMed2002

Therapies administered to mothers at risk for preterm birth and neurodevelopmental outcome in their infants.

A decrease in the rate of preterm births and the prevention of prematurity-associated neurodevelopmental morbidity are critical for the reduction of neurodevelopmental disability. Efforts to reduce the overall preterm delivery rate have been unsuccessful. Although progress has been achieved in the prevention of short-term neonatal morbidity over the past several decades, the majority of the improvements have resulted from improved neonatal care. Whether obstetric interventions can improve neurodevelopmental outcome is unknown. The ability to adequately assess obstetric interventions is hampered by the limited number of interventional studies that included long-term outcome assessment. Thus, it is incumbent upon ongoing and future interventional studies to consider long-term outcome assessment as a critical component of the overall evaluation of efficacy of obstetric therapies.

Anti-Bacterial Agents↗
PubMed2002

Effect of high dietary manganese intake of neonatal rats on tissue mineral accumulation, striatal dopamine levels, and neurodevelopmental status.

Mn is an essential element, but may become neurotoxic at high levels. Recent reports of high Mn levels in hair of children with neurodevelopmental deficits suggest that these deficits could be due to Mn-induced neurotoxic effects on brain dopamine (DA) systems, although the mechanism is not well understood. Infant formulas contain considerably higher concentrations of Mn than human milk. Thus, formula-fed infants are exposed to high levels of Mn at a time when Mn homeostasis is incompletely developed. We studied the effects of dietary Mn supplementation of rat pups on tissue Mn accumulation, brain dopamine levels, infant neurodevelopmental status, and behavior at maturity. Newborn rats were supplemented daily with 0, 50, 250, or 500 microg Mn given orally from day 1 to day 20. Mineral analysis of small intestine and brain at day 14 showed a significant increase of tissue Mn in supplemented rats. Neurodevelopmental tests conducted at various ages showed significant delays as a function of Mn supplementation. At day 32, there was a significant positive relationship between passive avoidance errors and Mn supplementation levels. Brains of animals killed on day 40 showed a significant inverse relationship between Mn supplementation level and striatal dopamine concentration. These observations suggest that dietary exposure to high levels of Mn during infancy can be neurotoxic to rat pups and result in developmental deficits.

Animals↗
PubMed2002

PCB-induced neurodevelopmental toxicity in human infants and its potential mediation by endocrine dysfunction.

Polychlorinated biphenyls (PCBs) cross the placenta and expose the fetus to the body burden of the mother. Additionally, the breastfed baby is postnatally exposed to PCBs in maternal milk. Among the broad spectrum of biological effects interaction with endocrine systems and developmental neurotoxicity are prominent features of these chemical mixtures. Associations between neurodevelopmental delay and prenatal or early postnatal PCB-exposure at environmental levels have been reported in several cohort studies. Adverse effects were found to be associated with early developmental PCB-exposure, although there are discrepancies between studies in terms of confounding, effective PCB-matrix, as well as spectrum and persistence of effects. From these cohort studies alone the causative role of PCBs in producing neurodevelopmental adversity still cannot be considered proven, but experimental findings do provide evidence for the developmental neurotoxicity of PCBs. The underlying mechanisms of this action is still unknown. However, interaction with endocrine systems, namely the estrogen/androgen and, particularly, the thyroid hormone systems are discussed as a possible explanation for PCB-induced neurodevelopmental adversity. Some evidence in this respect is being reviewed.

Adult↗
PubMed2001

Perinatal risk factors for adverse neurodevelopmental outcome after spontaneous preterm birth.

OBJECTIVE: The aim of this study was to investigate to what extend perinatal factors contribute to the neurodevelopmental outcome in a group neonates born after spontaneous preterm labour with or without prolonged rupture of the membranes (PROM). METHODS: In a cohort of neonates born after the spontaneous onset of labour with or without PROM before 34 weeks of gestation a stepwise forward logistic regression was performed to analyse the influence of antenatal and postnatal variables on adverse outcome. Adverse neurodevelopmental outcome was defined as a Griffith's developmental score <85, cerebral palsy, a major disability or perinatal death associated with severe cerebral damage. RESULTS: The study group consisted of 185 neonates. Seven neonates died with severe cerebral damage. After a forward logistic regression analysis three factors appeared to have an independent influence: gestational age protected against an adverse outcome (odds ratio (OR) per day increase 0.95, 95% confidence interval (CI) 0.90-0.97) while abnormal cranial ultrasound (intraventricular haemorrhage and periventricular leucomalacia) (OR 6.33, 95% CI 2.16-18.52) and the need for a second course of antibiotics (OR 1.85, 95% CI 1.02-3.33) increased the risk for adverse outcome. Comparing the group with a normal neurodevelopmental outcome with those with cerebral palsy, cranial ultrasound abnormalities were independently associated with cerebral palsy (OR 48.75, 95% CI 11.78-201.76). CONCLUSION: The most important way of preventing neurological damage in infants is to increase gestational age at birth and to avoid the development of intraventricular haemorrhage and periventricular leucomalacia.

Anti-Bacterial Agents↗
PubMed1999

Atrophic and static (neurodevelopmental) schizophrenic psychoses: premorbid functioning, symptoms and neuroleptic response.

The question of whether schizophrenic-like disorders are neurodevelopmental or degenerative in origin has been argued since the time of Kraepelin. The authors provide evidence for the existence of two etiologically distinct endophenotypes of the psychoses contained within the rubric of familial non-affective psychosis (schizophrenia), one atrophic and the other neurodevelopmental. The atrophic psychosis, identified by progressive ventricular enlargement throughout adult illness, evidences progressive impairment of interests, relationships, and withdrawal from latency through adolescence, with emergence of trait-like negative symptoms which are only marginally responsive to conventional neuroleptics. This psychosis also exhibits delayed response of positive symptoms during neuroleptic treatment, and may also proceed to a praecox dementia in later life. In contrast, a putative neurodevelopmental psychosis, associated with static ventricles during the course of adult illness, also demonstrates preadolescent impairments, but impairments which do not progress to marked negative symptoms. Conventional neuroleptics appear to have little effect (except sedation) on positive symptoms, but appear to induce negative symptomatology and partial disengagement from the burden of persistent psychotic thought processes in such static ventricle psychoses. Thus, separate patterns of illnesses with different prodromal features, different treatment response patterns, and different patterns of residual (negative) symptoms appear to characterize patients with psychosis who have expanding as opposed to stable cerebral-ventricles at doses of neuroleptic at 10 mg haloperidol equivalents/day.

Adult↗
PubMedDate not supplied

Validation of a new method for estimating resting energy expenditure of non-ambulatory tube-fed patients with severe neurodevelopmental disabilities.

OBJECTIVE: We assessed the bias and precision of the Arlington Developmental Center (ADC) equations derived from our previous study and the Harris-Benedict equations for estimating resting energy expenditure in non-ambulatory, tube-fed patients with severe neurodevelopmental disabilities. METHODS: Fifteen non-ambulatory patients with neurodevelopmental disabilities referred to the nutrition consult service for evaluation of enteral tube feeding via a permanent ostomy who had a steady-state resting energy expenditure measurement performed by indirect calorimetry were included in the study. The predicted energy expenditure values were compared with the measured resting energy expenditure values and evaluated for bias and precision. RESULTS: Both ADC equations were more precise (95% confidence interval [CI]: 9-22% and 10-18% error, respectively) for the total population than the Harris-Benedict equations (95% CI: 17-40% error). The ADC-2 equation was precise (95% CI: 7-15% error) and unbiased (95% CI: -5 to 139 kcal/d) in contrast to the Harris-Benedict equations (95% CI: 23-54% error; bias, +230 to 365 kcal/d) for patients with cerebral palsy and fixed upper extremity contractures. The Harris-Benedict equations were precise and unbiased (95% CI: 3-14% error; bias, -182 to 39 kcal/d) for patients with cerebral palsy with preservation of upper body movement, whereas the ADC equations were biased toward underprediction and associated with greater error (95% CI: -367 to -73 kcal/d and 7-26% error; 95% CI: -379 to -109 kcal/d and 9-27% error, respectively). CONCLUSIONS: The ADC-2 equation was unbiased and more precise in non-ambulatory adult patients with severe neurodevelopmental disabilities and fixed upper extremity contractures, whereas the Harris-Benedict equations were more precise and unbiased for those with preservation of limited functional and non-functional upper extremity movement.

Adolescent↗
PubMed2003

Attenuated stress responsiveness in an animal model for neurodevelopmental psychopathological disorders.

Day 7 amygdala-lesioned (D7 AMX) rats have been proposed as a model for neurodevelopmental psychopathological disorders such as schizophrenia. Patients with schizophrenia are sensitive to stress and show an impaired hypothalamic-pituitary-adrenal response to certain stressful stimuli. Therefore, we investigated neuroendocrine and behavioral stress responses in the D7 AMX lesion model. Plasma concentrations of ACTH, corticosterone, and catecholamines were measured in response to foot shock and novelty in D7 and D21 lesioned (AMX) and non-lesioned (SHAM) animals. Behavior was recorded and analyzed afterwards. D7 AMX rats, unlike other rats, had a reduced ACTH response to foot shock and showed less active behavior in response to novelty. Neurodevelopmental dysfunction of target structures of the amygdala is associated with disturbed endocrine and behavioral responses to stress. These data accord with the notion that the D7 amygdala-lesioned rat can function as a neurodevelopmental model with relevance to schizophrenia.

Adrenocorticotropic Hormone↗
PubMed2003

Neurodevelopmental vulnerability of the corpus callosum to childhood onset localization-related epilepsy.

Recent research has suggested that childhood onset of localization-related (focal) temporal lobe epilepsy is associated with a generalized adverse effect on cognition and brain structure, especially cerebral white matter volume. This study examined the neurodevelopmental impact of childhood onset epilepsy on corpus callosum volume and the cognitive consequences of reduced cerebral connectivity. Healthy controls (n = 15) and patients with temporal lobe epilepsy (n = 32) were matched on gender and handedness, and childhood and adult onset epilepsy groups were matched on duration of epilepsy (mean = 19 years) but varied in neurodevelopmental age at onset of recurrent seizures. Results showed that childhood onset of temporal lobe epilepsy was associated with significant volumetric reduction of the corpus callosum compared to both late onset and healthy controls, with the latter two groups not differing from one another. The volumetric loss was most evident in posterior followed by anterior corpus callosum. Volumetric reduction of the corpus callosum in temporal lobe epilepsy was of clinical significance with smaller volumes associated with poorer performance on measures of nonverbal problem solving, immediate memory, speeded complex psychomotor ability and fine motor dexterity. These findings indicate that childhood onset of temporal lobe epilepsy is associated with an adverse neurodevelopmental impact on brain connectivity which is of clinical consequence and theoretical interest.

Adolescent↗
PubMed2004

Systematic review of melatonin treatment in children with neurodevelopmental disabilities and sleep impairment.

Sleep disturbances in children with neurodevelopmental disabilities are common and frequently difficult to treat with conventional pharmacological and behavioural methods. Melatonin is a pineal hormone known to be important in the regulation of the circadian rhythm, including the sleep-wake cycle. This systematic review of available evidence from randomized clinical trials assesses whether melatonin plays a beneficial role in these children and, in particular, its effect on total sleep time, time to sleep onset (sleep latency), and number of awakenings. We also looked at a parental view of the effect. Randomized clinical trials were identified where oral melatonin was compared with a placebo in children with any type of neurodevelopmental disability and associated sleep disturbance. Only three studies, reporting a total of 35 children, fulfilled the criteria for inclusion. The two studies that reported time to sleep onset showed a significant decrease (p<0.05) in this specific outcome where melatonin was compared with a placebo. There was no significant effect of melatonin compared with a placebo on the other outcome measures of total sleep time, night-time awakenings, and parental opinions. Despite the extremely limited randomized clinical trial data, melatonin appears to remain a commonly prescribed drug for disturbed sleep in children with neurodevelopmental abnormalities.

Antioxidants↗
PubMed2000

The neurodevelopmental hypothesis of schizophrenia: following a trail of evidence from cradle to grave.

This is a critical review of the literature related to the neurodevelopmental hypothesis of schizophrenia which posits that the illness is related to abnormal brain development. The review focuses on data deriving from clinical studies, and it is organized according to the life phase from which the data were collected: conception and birth, infancy and childhood up to the onset of the illness, after illness onset, and postmortem. The neurodevelopmental hypothesis is supported by several pieces of evidence, including increased frequency of obstetric complications in patients with schizophrenia: the presence of minor physical anomalies; the presence of neurological, cognitive, and behavioral dysfunction long before illness onset; a course and outcome of the illness itself that is incompatible in most cases with a degenerative illness; the stability of brain structural measures over time; and the absence of postmortem evidence of neurodegeneration. A historical perspective on how this research accumulated and a section addressing important areas of future investigation are also provided. We conclude that schizophrenia is certainly not a degenerative brain disorder, and that it is likely that a brain insult in utero or at birth plays a role in its expression. Current evidence cannot completely exclude the role of environmental variables after birth. In addition, it is possible that other psychiatric disorders may also have a neurodevelopmental component.

Adolescent↗
PubMed2002

Neurodevelopmental outcome in high-risk patients after renal transplantation in early childhood.

Patient and graft survival rates of pediatric renal transplant recipients are currently excellent, but there are few reports regarding the long-term neurodevelopmental outcome after renal transplantation (Tx) in early childhood. Children with renal failure from infancy would be expected to have a less favorable developmental prognosis. We report the neurodevelopmental outcome in 33 school-age children transplanted between 1987 and 1995 when < 5 yr of age. We prospectively performed a neurological examination, magnetic resonance imaging (MRI) of the brain, electroencephalograms (EEGs), audiometry, and neuropsychological tests (NEPSY), and measured cognitive performance (WISC-R); we related these results to school performance and to retrospective risk factors prior to Tx. Twenty-six (79%) children attended normal school and 76% had normal motor performance. Six of the seven children attending a special school had brain infarcts on MRI. The EEG was abnormal in 11 (35%), and five (15%) received anti-convulsive treatment after Tx. Sensorineural hearing loss was documented in six patients. The mean intelligence quotient (IQ) was 87, and 6-24% showed impairment in neuropsychological tests. The children attending a special school had been more premature, but had not had a greater number of pre- or neonatal complications. They had experienced a greater number of hypertensive crises (p = 0.002) and seizures (p = 0.03), mainly during dialysis, but the number of septic infections and the mean serum aluminum levels were not significantly greater than in the children with normal school performance. In these previously lethal diseases, the overall neurodevelopmental outcome is reassuring. However, it is of crucial importance to further minimize the risk factors prior to Tx.

Audiometry↗
PubMed2023

Bi-allelic ATG4D variants are associated with a neurodevelopmental disorder characterized by speech and motor impairment.

Autophagy regulates the degradation of damaged organelles and protein aggregates, and is critical for neuronal development, homeostasis, and maintenance, yet few neurodevelopmental disorders have been associated with pathogenic variants in genes encoding autophagy-related proteins. We report three individuals from two unrelated families with a neurodevelopmental disorder characterized by speech and motor impairment, and similar facial characteristics. Rare, conserved, bi-allelic variants were identified in ATG4D, encoding one of four ATG4 cysteine proteases important for autophagosome biogenesis, a hallmark of autophagy. Autophagosome biogenesis and induction of autophagy were intact in cells from affected individuals. However, studies evaluating the predominant substrate of ATG4D, GABARAPL1, demonstrated that three of the four ATG4D patient variants functionally impair ATG4D activity. GABARAPL1 is cleaved or "primed" by ATG4D and an in vitro GABARAPL1 priming assay revealed decreased priming activity for three of the four ATG4D variants. Furthermore, a rescue experiment performed in an ATG4 tetra knockout cell line, in which all four ATG4 isoforms were knocked out by gene editing, showed decreased GABARAPL1 priming activity for the two ATG4D missense variants located in the cysteine protease domain required for priming, suggesting that these variants impair the function of ATG4D. The clinical, bioinformatic, and functional data suggest that bi-allelic loss-of-function variants in ATG4D contribute to the pathogenesis of this syndromic neurodevelopmental disorder.

Journal Article↗
PubMedDate not supplied

Ultrasonographic differential diagnosis and neurodevelopmental outcome of cerebral white matter lesions in premature infants.

OBJECTIVE: To determine the clinical usefulness of recently published ultrasonographic criteria for the differential diagnosis of periventricular hemorrhagic venous infarction (PHVI) versus periventricular leukomalacia (PVL), and its relevance to neurodevelopmental outcome. STUDY DESIGN: From 1992 to 1995, we evaluated 998 very low birth weight infants of which 111 developed cerebral white matter lesions on cranial ultrasonogram examination. An attempt was made to differentiate the lesions into either PHVI or PVL using specific ultrasonographic criteria (Volpe JJ. Brain inury in the premature infant: is it preventable? Pediatr Res 1990; 6:S28-33). Seventy-six patients who survived to discharge constituted the study group. Survivors were followed prospectively with neurologic examinations, visual and auditory screening, and developmental testing. RESULTS: PHVI was diagnosed in 23 patients (30%), PVL in 36 (47%), characteristics of both PHVI and PVL (mixed lesions) in 8 (11%), and persistent periventricular echodensity without cystic change in 9 (12%). Two-year follow-up data were obtained on 57 of 76 (75%) patients. Neurodevelopmental deficits were common in all groups; however, infants with localized PHVI had a mean developmental quotient in the normal range. CONCLUSION: The majority of white matter lesions (77%) can be differentiated as either PHVI or PVL by ultrasonographic criteria, with coexisting features in only 11% of patients. In addition to these lesions, persistent periventricular echodensity was also associated with a high risk of subsequent neurodevelopmental deficit. However, normal development was seen in a subgroup of patients with localized periventricular hemorrhagic venous infarction.

Brain Infarction↗
PubMed1999

Survival, intracranial lesions, and neurodevelopmental outcome in infants with congenital diaphragmatic hernia treated with extracorporeal membrane oxygenation.

OBJECTIVE: Before the use of extracorporeal membrane oxygenation (ECMO), infants with a severe form of congenital diaphragmatic hernia (CDH) had a high mortality and morbidity. Recent studies have shown an improvement in the survival of these infants after ECMO treatment; however, the existing data do not provide sufficient informations regarding the quality of survival and developmental outcome of these infants. The objective of this study was to evaluate survival, intracranial lesions, and the neurodevelopmental outcome of infants with CDH treated with ECMO. METHODS: We retrieved data for 51 (n = 51) infants with CDH who were treated with ECMO at Huntington Memorial Hospital between 1985 and 1994. Their mean gestational age was 38.5 +/- 2.4 weeks (mean +/- SD); their mean birth weight was 3170 +/- 620 gm. Vital signs, arterial blood gases, chest radiographs, cranial and cardiac ultrasonography were routinely obtained before ECMO treatment. Cranial ultrasounds were performed daily on all infants while on ECMO; computerized tomography scans were obtained on all infants after completion of ECMO treatment. The surviving infants were followed at our neonatal follow-up clinic for neurodevelopmental assessment. RESULTS: A total of 39 infants were placed on venoarterial ECMO and 12 infants were placed on venovenous ECMO; a total of 35 infants had CDH repair before ECMO, whereas 16 infants had delayed surgery. A total of 31 infants (61%) survived. The infants who survived had a mean pH of 7.33 +/- 0.20, mean airway pressure of 19.6 +/- 5.8 cm H2O, and an oxygenation index (OI) of 87 +/- 55 before ECMO intervention. The infants who expired (n = 20) had a mean pH of 7.31 +/- 0.15, mean airway pressure of 23.1 +/- 5.5 cm H2O, and a mean oxygenation index of 127 +/- 56 before ECMO treatment. Before ECMO, survivors had a significantly lower oxygenation index and a higher Pao2 compared with nonsurvivors (p < 0.01). A total of 18 infants (35%) had abnormal central nervous system findings. Of the 51 infants, 10 had ventricular dilatation, 6 had intracranial hemorrhage, and 11 had focal or diffuse cerebral atrophy diagnosed by computerized tomography scan or at autopsy (1 patient had an infarct). Eight infants had more than one central nervous system abnormality. A total of 16 survivors had a neurodevelopmental evaluation at 12 months, and 11 of these survivors were evaluated at 24 months of age (Bayley Scales of Infant Development). The developmental progress of these infants falls within the low-average range of cognitive and motor abilities. Their mean Bayley Mental Developmental Index was 85 +/- 25 (50 to 145) at 24 months; their Psychomotor Developmental Index was 89 +/- 21 (50 to 113) at 24 months of age. Follow-up at 4 and 6 years of age is in progress. CONCLUSION: Our preliminary findings indicate that 35% of infants with severe CDH requiring ECMO had central nervous system abnormalities (intracranial lesions, including ventricular dilatation). The survival rate in our study population is consistent with recent reports. As a group, infants with severe CDH display mild neuromotor and cognitive delay in development at 24 months of age.

Brain Diseases↗
PubMedDate not supplied

Neurodevelopmental and health outcomes in term infants treated with surfactant for severe respiratory failure.

OBJECTIVE: Analysis of health, neurodevelopmental, and school performance outcomes in a pilot study of term and near-term infants with respiratory failure due to pneumonia or meconium aspiration treated with surfactant. STUDY DESIGN: Retrospective review of medical records, neurodevelopmental and psychosocial evaluations, and parent and teacher surveys. RESULTS: Of the 14 patients enrolled, only one was rehospitalized, for pneumonia. Three were reported to have episodes of wheezing, two of whom required bronchodilators. One patient had unilateral hearing loss, one had a full-scale intelligence quotient that was below normal, and all but one patient for whom complete results were obtained were performing at or above grade level. CONCLUSION: Term and near-term newborns with moderately severe respiratory failure treated with surfactant can, in general, be expected to recover completely and have normal general health, neurodevelopmental outcome, and school performance.

Achievement↗