Cerebral Palsy In Term Infants Research Articles

Genomic analysis of presumed perinatal stroke in Saudi Arabia reveals a strong monogenic contribution.

Perinatal stroke is associated with significant short- and long-term morbidity and has been recognized as the most common cause of cerebral palsy in term infants. The diagnosis of presumed perinatal stroke (PPS) is made in children who present with neurological deficit and/or seizures attributable to focal chronic infarction on neuroimaging and have uneventful neonatal history. The underlying mechanism of presumed perinatal stroke remains unknown and thorough investigation of potential monogenic causes has not been conducted to date. Here, we describe the use of untargeted exome sequencing to investigate a cohort of eight patients from six families with PPS. A likely deleterious variant was identified in four families. These include the well-established risk genes COL4A2 and JAM3. In addition, we report the first independent confirmation of the recently described link between ESAM and perinatal stroke. Our data also highlight NID1 as a candidate gene for the condition. This study suggests that monogenic disorders are important contributors to the pathogenesis of PPSand should be investigated by untargeted sequencing especially when traditional risk factors are excluded.

Abstract WP175: A National, Population Based Study Of Neonatal Hemorrhagic And Ischemic Stroke

Background: Neonatal stroke occurs in an estimated 1 in 3000 live births and is the most common cause of hemiplegic cerebral palsy in term infants. Most population based studies on neonatal stroke in the past have been single center or regional, focused only on ischemic stroke, and with less than 100 cases. Large administrative datasets can provide information on comorbid perinatal conditions in neonatal stroke. Methods: Data for patients aged 0-28 days with a diagnosis of either ischemic or hemorrhagic stroke (either subarachnoid or intracerebral hemorrhage) were extracted from the Cerner Health Facts EMR database from 2000-2018. Incidence of birth demographics, perinatal complications, anti-epileptic use, and aspirin use was assessed. Odds ratios were calculated against a cohort of neonates without stroke. Results: Among 1,591,104 neonates in the Cerner EMR database, 452 (59%) neonates were identified with ischemic stroke and 311 (41%) with hemorrhagic stroke. The most common comorbidities for ischemic stroke were neonatal sepsis (16%, OR=13.1), head and scalp birth injury (13%, OR=7.1) and hypoxic injury (12%, OR=38.7). The most common comorbidities for hemorrhagic stroke were head and scalp birth injury (30%, OR=19.5), prematurity (26%, OR=4.2) and neonatal sepsis (23%, OR=13.1). Procedure codes for intubation, neonatal resuscitation, and epinephrine use were prominent in both hemorrhagic (15.1%, OR=35) and ischemic stroke (8.9%, OR=19.1). The proportion of hemorrhagic and ischemic stroke patients receiving antiepileptics was 23% and 27%, respectively. The proportion of ischemic stroke patients who received aspirin was 16.4%. Conclusion: This population based study of neonatal stroke, the largest of its kind, demonstrated a wide variety of comorbid conditions with ischemic and hemorrhagic stroke. Antiepileptic use is common in neonatal ischemic stroke, though in our population-based study of both academic and non-academic centers the prevalence is less than prior estimates. Sepsis, head and scalp injuries, prematurity, and hypoxic injury are associated with neonatal hemorrhagic and ischemic stroke, though prevalence varies between types. More study is needed on specific risk factors and pathogenesis in neonatal stroke.

Decline in severe spastic cerebral palsy at term in Denmark 1999-2007.

To analyse trends in prevalence and severity of cerebral palsy (CP) in Denmark in birth years 1999-2007 and compare with previous periods. Data has been collected uniformly in the Danish cerebral palsy national register nationwide since 1995. Rates in the time periods 1999-2001, 2002-2004 and 2005-2007 covering 585,393 births were analysed by gestational age and subtypes. Total number of CP cases in the period was 1165. The overall prevalence of CP decreased significantly from 2.1 in 1999-2001 to 1.8 in 2005-2007 per 1000 livebirths (p=0.022). The decline was only significant for children born at term (p=0.007) but not for the preterm (p=0.44). The decline in children born at term was based on a decrease in bilateral spastic CP (n=117 in years 1999-2001 and n=59 in 2005-2007). Multidisciplinary obstetric skills training with neonatal resuscitation in Denmark was initiated in 2003 and timely associated with the decrease. The prevalence of unilateral spastic CP the prevalence did not change, but in the two last time periods more children had a right-sided than left-sided unilateral spastic CP. The decline in rate of CP seen in 2005-2007 as compared to 1999-2001 was mainly based on fewer cases of severe spastic CP in term infants. We hypothesize that improved neonatal resuscitation in the delivery room may be partly responsible for the decrease. In premature children the decline was not significant in this time period, but has been dramatically decreasing in the years before the time period here analysed.

Are 1st-trimester β-human chorionic gonadotrophin and pregnancy-associated plasma protein A levels predictive of intrapartum fetal compromise in a selected normal population?

The incidence of cerebral palsy in term infants has not changed over the last 30years. Current intrapartum monitoring techniques are limited by their inherent poor specificity. Changes in fetal haemodynamics in the term fetus, similar to those seen in fetal growth restriction, have been associated with an increased risk of subsequent intrapartum fetal compromise. Alterations in first-trimester β-hCG and PAPP-A levels are predictive of fetal growth restriction. In this study, we aimed to establish whether first-trimester β-hCG and PAPP-A levels were predictive of fetal compromise in labour and whether these first-trimester markers could be correlated with fetal haemodynamics at term in a low-risk population. Over a two-year period, 427 women with low risk, uncomplicated pregnancies were recruited to this study. All participants underwent a prelabour ultrasound examination during which fetal biometry and haemodynamics were assessed. First-trimester β-hCG and PAPP-A levels were recorded from the case notes. All cases were followed up within 48hours of delivery, and first-trimester β-hCG and PAPP-A levels correlated with intrapartum outcomes and fetal haemodynamics. No significant relationship between first-trimester β-hCG and PAPP-A levels and subsequent intrapartum fetal compromise was observed. Weak but significant correlations were observed between β-hCG levels and umbilical venous flow rate, as well as PAPP-A levels and uterine artery pulsatility index. β-hCG and PAPP-A levels measured during the first trimester are not predictive of subsequent intrapartum fetal compromise within a low-risk population.

Interleukin‐6 genotype and risk for cerebral palsy in term and near‐term infants

Chorioamnionitis is associated with increased risk for cerebral palsy (CP) in term infants. A functional polymorphism in the interleukin-6 (IL-6) gene has been implicated in newborn brain injury. We studied whether the IL-6 -174 G/C polymorphism confers increased risk for CP in term infants. This population-based case-control study included 334,333 live-born infants born at >or=36 weeks gestation within Kaiser Permanente Medical Care Program from 1991 to 2002. Case patients (n = 250) were identified from electronic records and confirmed by chart review, and comprised all infants with spastic or dyskinetic CP not caused by developmental abnormalities who had a neonatal blood specimen available for study. Control patients (n = 305) were randomly selected from the study population. Compared with genotype GG, the less common CC genotype was associated with increased risk for overall CP (odds ratio [OR], 2.6; 95% confidence interval [CI], 1.5-4.6), quadriparetic CP (OR, 4.1; 95% CI, 1.8-9.3), and hemiparetic CP (OR, 2.7; 95% CI, 1.3-5.7), after controlling for race. The C allele conferred increased risk for CP in both recessive and additive genetic models. In multivariate analysis controlling for race, independent risk factors for CP included CC genotype compared with GG (OR, 2.4; 95% CI, 1.3-4.4), clinical chorioamnionitis (OR, 4.6; 95% CI, 2.1-10.4), maternal age >or= 35 (OR, 2.6; 95% CI, 1.6-4.1), and male sex (OR, 1.6; 95% CI, 1.1-2.4). Our data suggest that a functional polymorphism in the IL-6 gene is a risk factor for CP among term and near-term infants.

Prevalence, type, distribution, and severity of cerebral palsy in relation to gestational age: a meta‐analytic review

The aim of this review is to determine the relationship between gestational age (GA) and prevalence, type, distribution, and severity of cerebral palsy (CP). Epidemiological studies with cohorts expressed by GA were assessed. A comprehensive meta-analysis and meta-regression was performed on four fetal age categories. Studies of children with CP as a target population were added. Twenty-six articles met the inclusion criteria. The prevalence of CP decreases significantly with increasing GA category: 14.6% at 22 to 27 weeks' gestation, 6.2% at 28 to 31 weeks, 0.7% at 32 to 36 weeks, and 0.1% in term infants. Interestingly, a significant decrease in prevalence of CP starts only from a GA of 27 weeks onwards. In preterm infants, spastic CP is predominant. In term infants, the non-spastic form of CP is more prevalent than in preterm infants. Bilateral spastic CP is most prevalent in both preterm and term infants. However, the proportion of unilateral spastic CP in term infants is substantial. No relationship could be detected between severity of CP and GA. There is a strong need for an international, well-described, and generally accepted classification system for subtypes and severity of CP.

Perinatal Factors Associated With Cerebral Palsy in Children Born in Sweden

To identify perinatal factors associated with cerebral palsy (CP). This was a case-control study based on the Swedish Medical Birth Registry and the Swedish Hospital Discharge Registry, including 2,303 infants born in Sweden 1984-1998 with a diagnosis of CP and 1.6 million infants without this diagnosis. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Infants born preterm had a highly increased risk for CP, and constituted 35% of all cases; OR 34 (95% CI 29-39) in weeks 23-27, OR 37 (95% CI 32-42) in weeks 28-29, OR 26 (95% CI 23-30) in weeks 30-31, and OR 3.9 (95% CI 3.4-4.4) in weeks 32-36. Boys had a higher risk (sex ratio 1.36:1), particularly before term (sex ratio 1.55:1). Other factors associated with CP were being small or large for gestational age at birth, abruptio placentae (OR 8.6, 95% CI 5.6-13.3), maternal insulin-dependent diabetes mellitus type 1 (OR 2.1, 95% CI 1.4-3.1), preeclampsia (OR 1.5, 95% CI 1.3-2.4), being a twin (OR 1.4, 95% CI 1.1-1.6), maternal age older than 40 years (OR 1.4, 95% CI 1.1-1.8) or 35-39 years (OR 1.2, 95% CI 1.1-1.4), primiparity (OR 1.2, 95% CI 1.1-1.3), and smoking (OR 1.2, 95% CI 1.1-1.3). In term infants, low Apgar scores were associated with a high risk for CP; OR 62 (95% CI 52-74) at score 6 at 5 minutes, OR 498 (95% CI 458-542) at score 3. Other factors associated with CP in term infants were breech presentation at vaginal birth (OR 3.0, 95% CI 2.4-3.7), instrumental delivery (OR 1.9, 95% CI 1.6-2.3), and emergency cesarean delivery (OR 1.8, 95% CI 1.6-2.0). Preterm birth entails a high risk for CP, but 65% of these children are born at term. Several obstetric factors and low Apgar scores are associated with CP. II-2.

Cerebral Palsy

Cerebral palsy (CP) is a group of disorders of movement and posture resulting from nonprogressive disturbances of the fetal or neonatal brain. More than 80% of cases of CP in term infants originate in the prenatal period; in premature infants, both prenatal or postnatal causes contribute. The most prevalent pathological lesion seen in CP is periventricular white matter injury (PWMI) resulting from vulnerability of the immature oligodendrocytes (pre-OLs) before 32 wk of gestation. PWMI is responsible for the spastic diplegia form of CP and a spectrum of cognitive and behavioral disorders. Oxidative stress and excitotoxicity resulting from excessive stimulation of ionotropic glutamate receptors on preOLs are the most prominent molecular mechanisms for PWMI. Asphyxia around the time of birth in term infants accounts for less than 15% of CP in developed countries but the incidence is higher in underdeveloped areas. Asphyxia causes a different pattern of brain injury and CP than is seen after preterm injuries. This type of CP is associated with the clinical syndrome of hypoxic-ischemic encephalopathy shortly after the insult, and the cortex, basal ganglia, and brainstem are selectively vulnerable to injury. Experimental models indicate that neurons in the neonatal brain are more likely to die by delayed apoptosis extending over days to weeks than those in the adult brain. Neurons die by glutamate-mediated excitotoxicity involving downstream caspase-dependent and caspase-independent cell death pathways. Recent reports indicate that males and females preferentially utilize different pathways. Clinical trials indicate that mild hypothermia reduces death or disability in term infants following asphyxia and basic research suggests that this approach might be combined with pharmacological strategies in the future.

Lesions of the basal ganglia and thalamus – the most frequent cause of cerebral palsy in term infants

Objectives: Parasagittal cortico-subcortical lesions (PCSL) and lesions of the basal ganglia and thalamus (BThL) are a typical lesion pattern of the term infant following hypoxic-ischaemic encephalopathy (1). In the context of the European Cerebral Palsy Study (a multicentre study with 6 participating European centres) we analysed magnetic resonance (MR) imaging studies of the brain in a systematic way. The MR findings were related to clinical data.

Chorioamnionitis and Cerebral Palsy in Term and Near-Term Infants

It is well known that preterm birth increases the risk of cerebral palsy (CP), but more than half of affected children are born at term and the prevalence of CP in term infants has not declined in recent years. Because there is evidence that chorioamnionitis could substantially raise the risk of CP

Maternal infection and cerebral palsy in term infants with periventricular leucomalacia

WITH PERIVENTRICULAR LEUCOMALACIA BO JACOBSSON, GUDRUN HAGBERG, HENRIK HAGBERG, Perinatal Center, Goteborg, Sweden Dept. of Pediatrics, Goteborg, Sweden OBJECTIVE: Previous studies have investigated maternal infection during delivery as a possible risk factor for cerebral palsy (CP) in term infants. Infants born at term with diagnosed CP and periventricular leukomalacia (PVL) have, however, been excluded. The aim of this study was to investigate the relationship between maternal infections during pregnancy and PVL combined with CP in the offspring. STUDY DESIGN: A population-based case-control study. Term infants with CP and PVL (CP/PVL) (n = 44) born in 1983-94 were included and matched with a control group (n = 88). All records were scrutinized for any infectious disease or use of antibiotics during pregnancy. Cystic and atrophic PVL were diagnosed by a computed tomographic scan. RESULTS: Mothers with any event of infectious disease noted in their records had an increased risk of having a child with CP/PVL (19/44 cases, 21/88 controls [OR 2.42 {1.12-5.25}]), and if the mothers had suffered any event of amore serious infectious disease during pregnancy, they had an even higher risk (6/44 cases, 1/88 controls [OR 13.74 {1.60-118}]). Apgar score < 7 at 1, 5, or 10 minutes did not constitute a risk factor for CP in this particular subgroup of infants. CONCLUSION: Infection in pregnant women was significantly associated with CP/PVL in term infants, especially in those pregnancies complicated by a more severe maternal infection. In spite of a previously demonstrated close correlation between Apgar score at birth and unexplained CP in term infants, depressed viability at birth did not confer an increased risk of CP/PVL. Speculatively, maternal infection during late mid-pregnancy may inflict fetal white matter injury, but not preterm birth, resulting in PVL/CP in infants born at term without signs of intrapartal asphyxia.

Cerebral palsy in term infants: a population-based case-control study of infectious antenatal and intrapartal risk factors

To analyze infection-related risk factors during pregnancy and delivery for spastic CP in infants born at term in a large case-control study. A population-based series of infants with spastic unexplained CP born at term (n = 166) between 1983 and 1994 were included and matched with a control group (n = 332). Maternal, antenatal, and intrapartal variables were retrieved from obstetric records, focusing on infectious factors defined in advance. In general, few episodes of fever were observed in the records, and only one case of clinical chorioamnionitis. Fever (≥38 degrees) before onset of the delivery (OR 1.01 [0.18-5.55]) or fever during the delivery (OR 1.02 [0.19-5.64]) was not associated with CP, but fever (≥38 degrees two times with at least 4 h apart) within 48 h after delivery was associated with CP (7/163 cases, 4/330 controls [OR 3.66 {1.055-12.68}]). Use of antibiotics before onset of delivery (OR 2.73 [0.60-12.36]) was not associated with CP, but use of antibiotics during delivery correlated with CP (8/157 cases, 0/311 controls [OR 16.64 {2.062-134.4}]). There was an association between any infectious disease during pregnancy and CP (59/166 cases, 77/332 controls [OR 1.82 {1.21-2.74}]), but we did not find an increased risk of CP among women having a more severe infection during pregnancy (OR 1.17 [0.45-3.04]). Bacteruria during pregnancy was related to CP (16/166 cases, 6/332 controls [OR 5.80 {2.22-15.1}]). Low viability at birth (Apgar<7 at 1, 5, and 10 minutes) constituted a high risk for unexplained CP in infants born at term. No clear association between fever or other infectious signs during delivery and CP were found in term infants. Fever post partum might have been recorded more accurately than during birth and might therefore represent an indicator of intrapartal infection. Any infectious disease or bacteruria noted in the mother's record during pregnancy constituted a moderately increased risk of CP.

Analysis by gestational age of cerebral palsy in singleton births in north-east England 1970-94.

We report from a well-established cerebral palsy (CP) register the changes in CP rates by gestational age for singleton births over a 25-year period in north-east England. The gestational ages of numerators and denominators are of high accuracy back to 1970 because academic units in paediatrics and obstetrics were studying the assessment of gestational age in individual infants, and the distribution of gestational age across all births in the north-east from the 1960s. The rate of CP rose between 1970-75 and 1990-94 from 1.6 to 2.3 per 1000 singleton neonatal survivors, a rise of 0.7/1000 [95% CI 0.2, 1.3]. There was little change in the rate of CP in term infants whereas in preterm infants (<37 weeks) it rose from 5.5 to 16.8, a rise of 11.3/1000 [95% CI 5.9, 16.8]. Rises occurred in the three preterm gestational age bands <28, 28-31, 32-36 weeks with the most marked rise in those <28 weeks from 0 to 112.7. The proportion of all cases of CP arising in the preterm group rose from 19% to 45%; and the proportion of the severest cases arising in the preterm group rose from 8% to 55%. In those born after 32 weeks, there is a preponderance of small-for-gestation infants, with 10% more than two standard deviations below the mean. All types of CP are more common in infants below average weight for gestation and this is most marked for the non-spastic types that are almost only seen in term, small-for-gestation infants. Gestational age is the crucial determinant of rate of CP and the increase in prevalence seen over the past 25 years is due to increased rates in preterm infants, not term infants. Both conclusions, suspected from birthweight analyses, are now demonstrated conclusively, with the contribution coming from those 32-36 weeks gestation as well as very preterm infants.

The epidemiology of cerebral palsy in term infants.

Half of cerebral palsy (CP) arises in infants of normal birthweight; yet, many fewer studies seek to identify risk factors for CP in term and near-term infants than in those born very prematurely. There has been no net decrease in the prevalence of CP in term and near-term infants over recent decades. Potentially asphyxiating birth complications account for a small minority of CP cases. Recent studies suggest that disorders of coagulation and intrauterine exposure to infection or inflammation are associated with risk of CP, and that both can be accompanied by signs of neonatal encephalopathy, the best available predictor of CP in term neonates. Therapeutic interventions directed at preventing interruption of oxygen supply have not been shown to reduce the occurrence of CP. There have not yet been studies examining whether medical interventions directed at infection or coagulation disorder can reduce the frequency of CP.

Public health issues related to infection in pregnancy and cerebral palsy.

Cerebral palsy is the most common neuromotor developmental disability of childhood, affecting as many as 8,000 to 12,000 children born in the U.S. each year (corresponding to a prevalence rate of between 2 and 3 per 1000 children). Recent improvements in neonatal care have not resulted in a decline in the overall prevalence of cerebral palsy and, in fact, greater numbers of very preterm/very low birth weight infants are surviving with cerebral palsy and other developmental problems. Infection in pregnancy may be an important cause of the disorder. In preterm infants, there appears to be about a 2-fold increased risk for cerebral palsy from chorioamnionitis, and in term infants the estimated increased risk is about 4-fold. Provisionally, chorioamnionitis might account for 12% of spastic cerebral palsy in term infants and 28% of cerebral palsy in preterm infants. Studies of biochemical markers of fetal inflammation typically associated with infection also suggest that an inflammatory response may be an important independent etiologic factor. If a substantial proportion of cerebral palsy is attributable to acute amnionitis infection and/or neonatal sepsis, cerebral palsy should have decreased in the United States after administration of intrapartum antibiotics became widespread in response to publication of public health consensus guidelines for Group B streptococcus in 1996. However, failure to detect declines could have a number of explanations and these explanations illustrate the many public health challenges related to intrauterine infection and cerebral palsy. Given the gaps in our current knowledge about intrauterine infection and cerebral palsy, public health recommendations for timely and specific prevention activities are limited at this time.

Cerebral palsy--medicolegal aspects.

In 1862 William James Little, a London orthopaedic surgeon wrote: ‘The object of this communication is to show that the act of birth does occasionally imprint upon the nervous and muscular systems of the nascent infantile organism very serious and peculiar evils. Nearly twenty years ago... I showed that premature birth, difficult labours, mechanical injuries during parturition to head and neck, where life had been saved, convulsions following the act of birth, were apt to be succeeded by a determinate affection of limbs of new-born children, spastic rigidity from asphyxia neonatorum, and assimilated it to the trismus nascentium and the universal spastic rigidity sometimes produced at later periods of existence1.’ This condition was known as Little's disease until William Osler coined the term cerebral palsy in 1888. He too noted the association with difficult deliveries and with asphyxia requiring prolonged resuscitation2. In the 1890s Sigmund Freud was the first to recognize that antepartum and postpartum factors could cause a similar condition. He postulated that most cases arose from difficult birth but speculated that the birth difficulty might have been caused by some underlying condition2. The asphyxia theory was subsequently given impetus when research in monkeys showed that perinatal asphyxia could cause brain damage3. In the past 30 years, great increases in the use of fetal monitoring and caesarean section have been driven by the belief that early detection of asphyxia and speedy delivery will prevent brain damage. In parallel with these changes there has been an unprecedented rise in malpractice litigation. Surprisingly, over the same period the incidence of cerebral palsy in term infants has not changed4,5. This lack of impact prompted epidemiological studies which showed that asphyxia accounts for less than 10% of cases6. In 1999 an international consensus statement was published to provide an agreed reference for use by the courts and expert witnesses in birth injury litigation7. The intention was to provide a template that could be modified as new knowledge became available8.

Cerebral palsy births in eastern Denmark, 1987--90: implications for neonatal care.

The Cerebral Palsy Register in eastern Denmark has collected cases using a uniform data sampling procedure since birth year 1979. We have investigated changes in the rate of cerebral palsy, related to gestational age, mortality and perinatal risk factors in children born 1983--90. The total cerebral palsy birth prevalence decreased from 3.0 in the birth year period 1983--86 to 2.4 per 1000 live births (P < 0.01) in 1987--90, owing to a decrease among all preterm infants (29--19 per 1000, P < 0.001). The perinatal and early neonatal mortality in preterm infants was unchanged from 1983--86 to 1987--90. The rate of cerebral palsy in term infants was 1.5 per 1000 in all birth-year periods from 1979--90. Among the cerebral palsy infants, the proportion of very preterm babies treated with mechanical ventilation in the neonatal period decreased from 95% in 1983--86 to 61% in 1987--90 (P < 0.001), while the group treated with CPAP among the moderately preterm babies increased from 61% to 78% (P < 0.05). The significant decline in cerebral palsy rate in preterm infants born 1987--90 may be due to a change in treatment at the neonatal intensive care units using less mechanical ventilation, a hypothesis which needs further investigation.

Cerebral palsy in term infants—birth or before birth?

Cerebral palsy in term infants—birth or before birth?

The relationships between neonatal encephalopathy and cerebral palsy: a cohort study

There is a high risk of cerebral palsy (CP) following neonatal encephalopathy (NE) with fits, often attributed to intrapartum asphyxia. The evidence for the association is inconclusive and antepartum factors offer an alternative explanation. A cohort study was carried out to assess the evidence for and against hypoxic ischaemic injury as the cause of NE-associated CP in term infants. A total of 57 159 consecutive births were enrolled. There were 150 cases with NE, of whom 92 had at least one fit and 58 had no fits. The incidence of all NE was 2·62 per 1000 births and of NE with fits was 1·61 per 1000 births. Infants with NE were followed-up to identify those with cerebral palsy. There were 13 cases of four-limb cerebral palsy and three with hemiplegia among the survivors. In 12 of the 13 cases of four-limb CP, a combination of low Apgar scores, an early onset acute evolving encephalopathy, acidosis, renal dysfunction and the absence of antepartum factors suggested an acute intrapartum event as the immediate cause of the NE. An obstetric event likely to cause acute hypoxic injury was identified in four of the 12 cases. The clinical picture was similar in the four with and the eight without a specific obstetric event. The pathway leading to NE-associated CP remains unexplained, but intrapartum events appear to play a major role in most cases.

THE NEUROLOGICALLY IMPAIRED CHILD AND ALLEGED MALPRACTICE AT BIRTH

Controlled studies, improved epidemiologic and statistical techniques, and an increase in biological information on mechanisms of fetal and neonatal brain injury or maldevelopment have led to a better, although still imperfect, understanding of the cause of developmental disabilities. The role of asphyxia during the birth process is smaller than was once believed. Intrauterine exposure to infection, autoimmune and coagulation disorders, and problems specific to multiple pregnancies are risk factors for cerebral palsy. Electronic fetal monitoring and other observations during birth are unsatisfactory management guides, having enormously high rates of false-positive identification. There is no evidence that caesarean section can prevent cerebral palsy in term infants.