Evaluation to See if My Baby Has Cerebral Palsy
Clin Obstet Gynecol. Author manuscript; available in PMC 2011 Mar ix.
Published in final edited form as:
PMCID: PMC3051278
NIHMSID: NIHMS107730
Diagnosis, Handling, and Prevention of Cerebral Palsy in About-Term/Term Infants
Abstract
Cerebral palsy is the most prevalent cause of persisting motor function damage. In a majority of cases, the predominant motor abnormality is spasticity; other forms of cerebral palsy include dyskinetic (dystonia or choreoathetosis) and ataxic cerebral palsy. The care of individuals with cerebral palsy should include the provision of a chief intendance medical home for care coordination and suppor and diagnostic evaluations. Current strategies to subtract the risk of cognitive palsy include interventions to prolong pregnancy (e.g., 17α-progesterone), limiting the number of multiple gestations related to assisted reproductive applied science, antenatal steroids for mothers expected to deliver prematurely, caffeine for extremely low birth weight neonates, and induced hypothermia for a subgroup of neonates diagnosed with hypoxic-ischemic encephalopathy.
Keywords: cognitive palsy, function impairment, neuroimaging classification, postnatal prevention
Introduction
Amid the variety of disorders that severely impair motor function in young children, cognitive palsy is the most prevalent. In birth cohorts from developed countries, the prevalence is ane-2/1000 live births(1). The prevalence rises dramatically with decreasing gestational age at birth such that among extremely low gestational age newborns (i.e., gestational age < 28 weeks), the prevalence is about 100 per thou of surviving infant, a 100-fold higher take a chance than infants built-in at term. Equally a function of all live births, the prevalence has been remarkably stable for decades, but this has not been the example amongst very low birth weight and very preterm infants, among whom prevalence increased after the introduction of neonatal intensive care and has begun to decrease in the by decade(one).
In addition to motor manifestations, children with cerebral palsy oftentimes exhibit cognitive and sensory impairments, epilepsy, and nutritional deficiencies. Except in the mildest cases, cerebral palsy has a substantial impact on families' well being and societal wellness care costs.
Every bit a outcome of both laboratory-based and clinical research over the past several decades, a few perinatal interventions have been identified which probably are constructive for lowering the risk of cerebral palsy. Successes from clinical inquiry on cognitive palsy has been enhanced by efforts to increase the reliability (and thereby validity) of the diagnosis and nomenclature of this disorder. These efforts take improved the efficiency of observational and experimental epidemiologic studies related to prevention, likewise as intervention trials for individuals with cerebral palsy.
In this manuscript I volition begin by reviewing research on the diagnosis and classification of cerebral palsy, including efforts to standardize diagnostic criteria, quantify severity in terms of motor harm and impact on quality of life, and classify children with regard to location and type of neurological abnormality, associated non-motor impairments, and neuroimaging findings. I will then discuss the care of individuals particularly, children, with cerebral palsy, with a principal focus on show from randomized trials. In final I volition discuss preventive interventions that announced likely to accept an impact on the risk of cerebral palsy or that are currently under study in clinical trials. While some of these interventions are not applicable to obstetric intendance, it is probable that all volition exist of involvement to obstetricians.
Diagnosis of Cerebral Palsy
The diagnosis of cerebral palsy is based on a clinical assessment, and not on laboratory testing or neuroimaging. A recent international working group offered the following definition for cerebral palsy: "Cerebral palsy is a grouping of permanent disorders of the development of motion and posture, causing activity limitation, that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain."(2) This definition allows for heterogeneity of clinical manifestations ("a grouping of ... disorders") and emphasizes that impaired motion and posture due to a disturbance in the brain is the invariant clinical manifestation. While the underlying abnormality of the brain is presumed to exist permanent and not-progressive, in that location is overwhelming testify that clinical manifestations and severity of functional damage often modify over fourth dimension. Thus from a patient'south perspective, the term "permanent" may connate an unduly pessimistic prognosis. In contrast to before definitions of cognitive palsy, that proposed by the aforementioned international working grouping included an explicit benchmark for the lower limit of abnormality that must be exceeded in order to diagnose CP, i.e., "activity limitation".
On the other manus, this working grouping did non offer a readily operational approach to the observation of activeness limitation. The approach that appears to exist most widely used is based on a standardized measure of motor function, the Gross Motor Function Classification System (GMFCS)(iii), which will be discussed below in greater particular. The GMFCS has been included in several recent randomized clinical trials as part of the definition of severity, and in these trials children with mild cerebral palsy without functional impairment were not considered to accept the outcome of interest. The Western Australian Cerebral Palsy Register grades severity using the GMFCS, which allows for researchers to include or exclude cases without functional damage. In an international study involving prematurely born children with cerebral palsy, "disabling", as opposed to "non-disabling" cerebral palsy was ascertained with greater reliability, suggesting that the exclusion of cases without functional impairment may ameliorate the validity of observational epidemiologic studies as well as randomized trials in which cerebral palsy is an outcome. Conversely, clinicians should regard with circumspection those studies of cerebral palsy in which information is lacking about the severity of cerebral palsy, as assessed with a reliable measure.
In clinical exercise, the diagnosis of cognitive palsy is typically based on observations or parent reports of attained motor milestones, such as sitting, pulling to stand, and walking, and evaluation of posture, deep tendon reflexes, and muscle tone. Especially among infants born prematurely, neurological abnormalities, observed in the early months of life, may not be associated with motor impairment and may resolve during the kickoff one or two years of life. I such abnormality, transient dystonia, was described in early studies of premature infants and refers to aberrant neurological signs (eastward.one thousand., hyperextension of the trunk) that are no longer present after ane year of age. Because the diagnosis of cerebral palsy depends in part on neurological findings that are bailiwick to inter-examiner variation, with regard to both the method used to arm-twist the neurological finding equally well as the estimation of the finding, and considering neurological abnormalities may exist transient, many clinicians avert basing the diagnosis on a single aspect of the parent's written report or the clinician's examination and typically will brand a definitive diagnosis only subsequently repeated test(s).
Considering cerebral palsy occurs in only 1-ii / 1000 live births, prospective ascertainment of cases has been limited primarily to cohorts of high hazard infants, such as low birth weight babies, very preterm infants, and infants enrolled in clinical trials. For population-based studies, registries of children with cognitive palsy have been used, such as those established in Sweden, Western Australia, Metropolitan Atlanta, and Europe. Children listed in these registries are identified from records of human services providers and in some studies the diagnosis is confirmed by examination of medical records or of the child. These population studies take been particularly informative most trends in prevalence over time.
In many recent studies of loftier chance infants(four-6), painstaking efforts were directed at standardizing the definition of cerebral palsy used for prospective identification. With some minor differences between studies, each of these studies base the definition on a combination of delayed motor development (either observed or parent-reported), deep tendon reflexes, posture, and muscle tone (see Figure 1). For more details the reader is directed to reference(7).
Decision tree for inclusion/exclusion of cases of cerebral palsy on SCPE annals. Reproduced with permission from Surveillance of Cognitive Palsy in Europe (SCPE). Surveillance of cerebral palsy in Europe: a collaboration of cognitive palsy surveys and registers. Dev Med Child Neurol 2000; 42: 816-824
For both clinical as well as enquiry purposes, cerebral palsy has often been classified according to the nature of the movement disorder (spasticity, ataxia, dystonia, and athetosis) and the anatomic, or topographic distribution of the motor abnormalities. The predominant abnormality amongst children born prematurely is spasticity, referring to a velocity dependent increase in muscle tone. Spasticity tin can be assessed clinically every bit the articulation angle at which an increase muscle tone (resistance to stretch) is encountered. In a much smaller proportion of cases, referred to as having dyskinetic cerebral palsy, the predominant abnormality is either dystonia or choreo-athetosis. Dystonia refers to hypertonia and reduced activity; choreoathetosis, to irregular, spasmodic, involuntary movements of the limbs or facial muscles. With ataxic cognitive palsy at that place is a loss of orderly muscular coordination, so that movements are performed with abnormal force, rhythm, and accuracy.
A traditional classification of children with spastic cerebral palsy includes spastic diplegia (bilateral spasticity with leg interest greater than arm), spastic hemiplegia (unilateral spasticity), or quadriplegia (bilateral spasticity with arm involvement equal to or greater than leg). In a big population-based report of very low birth weight children with cerebral palsy, 25% of children with spastic CP had hemiplegia, 37.v% had quadriplegia, and 37.v% had diplegia. Children with hemiplegia nigh e'er develop independent ambulation, whereas a majority of those with quadriplegia do not. In that location is some evidence that the contour of risk factors differs for each of these topgraphic types of cerebral palsy. It should be noted, withal, that the inter-rater reliability of examiners' topographic classification is not high; thus the Surveillance for Cerebral Palsy in Europe (SCPE), a multi-center research collaboration, has proposed an alternative classification that includes unilateral spastic cognitive palsy, bilateral spastic cerebral palsy, dystonic cognitive palsy, choreo-athetoid cerebral palsy, and ataxia (see Effigy 2). Currently no method of topographic classification has been broadly agreed upon.
Hierarchical classification tree of cerebral palsy sub-types. Reproduced with permission from Surveillance of Cognitive Palsy in Europe (SCPE). Surveillance of cerebral palsy in Europe: a collaboration of cerebral palsy surveys and registers. Dev Med Kid Neurol 2000; 42: 816-824
More understanding has been achieved on classification of cognitive palsy in terms of the functional severity. More a decade agone, Palisano and his colleagues adult the GMFCS, which defines five levels of gross motor function, which have been shown to stand for to five distinct "trajectories" of motor development. For example, among children younger than ii years, those at level II tin "maintain floor sitting but may need to use their hands for support to maintain balance," whereas those at level Four accept head command simply trunk support is required for floor sitting". The GMFCS correlates strongly with the Globe Health Organization International Classification of Impairments, Disabilities and Handicap code, simply is considerably less time-consuming and can exist derived from medical records. The inter-rater reliability of the GMFCS is high, as is the stability over time. The GMFCS level of children, as reported by parents, agrees well with that assigned by a physician; and the level self-reported by adults agrees well with that assigned by a physical therapist..
Other assessments have been developed for fine motor part, including the ABILHAND-Kids, the Bimanual Fine Motor Function (BFMF) Classification, and the Manual Ability Classification System. These assessments accept non been studied equally extensively as the GMFCS, but in ane study the BFMF correlated strongly with the GMFCS, and in another, a high level of agreement nearly the MACS was found between pairs of therapists. Thus a comprehensive description of an individual with cognitive palsy would include both the GMFCS also as a measure out of upper extremity (fine motor) function.
In a large proportion of individuals with cognitive palsy, the motor impairment is accompanied by secondary musculoskeletal bug, epilepsy, and disturbances of sensation, perception, cognition, communication, and behavior(8). Among children registered in the SCPE Collaboration, 31% take severe intellectual disability, 11% have severe visual disability, and 21% have epilepsy. The likelihood of associated impairments varies according to topographic type. Less than i half of children with leg dominant bilateral spastic cerebral palsy have mental retardation, which is nowadays in more than than 1 half of children with other forms of spastic cerebral palsy. Severe visual impairment is present in more one half of children with four leg dominant spastic CP only but less than 10% of children with two leg ascendant spastic cerebral palsy.
Quality of life has been divers as "an individual's perception of their position in life in the context of the culture and value systems in which they live, and in relation to their goals, expectations, standards and concerns." Using validated instruments which allow children to self-written report on their quality of life, researchers have found that most children with cerebral palsy report similar quality of life to children not affected with this disorder and that quality of life is not worse with greater levels of functional impairment(nine). In contrast, health related quality of life, which measures life satisfaction in areas such equally cocky-care, mobility, and advice is influenced by the severity of impairment.
Neuroimaging classification
Until recently, neuroimaging studies of preterm infants with cerebral palsy were based largely on neonatal cranial ultrasound. The most widely used classification system, derived from computed tomography but applied readily to ultrasound findings, was described by Papile et al. In this approach to classification, grade ane refers to hemorrhage limited to the subependymal germinal matrix region, form two refers to hemorrhage in the cerebral ventricule(s), grade 3 refers to hemorrhage in the ventricle(due south) with ventricular enlargement, and form 4 refers to hemorrhage in the periventricular cerebrum. More contempo approaches to classification, justified past extensive research, emphasize echolucency in the periventricular cerebrum and moderate-to-astringent ventricular enlargement as most predictive of subsequent cerebral palsy(10). Very low birth weight infants with either of these abnormalities have a greater than 50% risk of developing cerebral palsy. For more details see reference (xi)
Most children who are born at term and subsequently develop cerebral palsy do not undergo neuroimaging studies as neonates, but rather, after the diagnosis is suspected. Magnetic resonance imaging (MRI) is recommended for children with neurological findings suggestive of cerebral palsy in club to determine if a brain abnormality is present. In a study of 273 children with cerebral palsy who were born after 35 weeks gestation and underwent neuroimaging, one third of infants who underwent neuroimaging had normal studies(12). The nigh frequent observed abnormality was focal infarction, which was observed in 22% of the children and 45% of those with hemiplegia. The next almost common finding was brain malformation, including schizencephaly, hydrocephalus, polymigrogyria, lissenencephaly, agenesis of the cropus callosum, holoprosencephaly, septooptic dysplasia, and cerebellar anomalies. In 12% of children neuroimaging revealed periventricular leukomalacia, a finding frequently is associated with prematurity. Of note is that simply 5% of children had neuroimaging findings considered specific to hypoxia-ischemia(12).
Care of the child with cerebral palsy
Initial assessments (see Figure three) for children diagnosed with cerebral palsy include neuroimaging if the etiology has not been established and metabolic and genetic studies if clinical history and findings on neuroimaging practice not determine a specific etiology or if there are aspects of the history or physical examination that suggestive of a metabolic or genetic etiology (including a brain malformation). In addition, testing for prothrombotic abnormalities of coagulation should be considered in individuals with hemiplegia. All children with cerebral palsy should be screened for mental retardation, ophthalmologic and hearing impairment, and speech and linguistic communication disorders, and nutrition and growth should be monitored(13).
Alogorithm for evaluation of the child with cerebral palsy. Reprinted with permission from Ashwal S, Russman BS, Blasco PA, Miller G, Sandler A, Shevell Thou, Stevenson R; Quality Standards Subcommittee of the American University of Neurology; Practice Committee of the Kid Neurology Society. Practise parameter: diagnostic assessment of the child with cognitive palsy: report of the Quality Standards Subcommittee of the American University of Neurology and the Practice Committee of the Kid Neurology Society. Neurology. 2004 Mar 23;62(6):851-63
The American Academy of Pediatrics has emphasized the importance of a master care "medical habitation" for children with chronic illnesses, including cerebral palsy(8). The roles of the medical home include care coordination to minimize redundant services and assure comprehensive services, monitoring of response to treatments and bear on of the child'south disease on the family, interpreting findings to the family, orchestrating comanagment with specialists and specialty teams, and advocating for the patient with payers and providers such as the public schools(8). (Starting time in 1975, a series of United states of america public laws has specified that all handicapped children take available to them a complimentary appropriate education designed to meet their unique needs. The most contempo of these is Public Law 108-446, the Individuals with Disabilities Instruction Comeback Act of 2004.)
Every bit discussed above, a big majority of children with cognitive palsy have spasticity. Active management of spasticity is needed to foreclose painful contractures and deformities and promote optimal function. This management generally is provided by multidisciplinary teams that include physical therapists, orthopedic surgeons, and physiatrists. Concrete therapy, which is uniformly utilized for cerebral palsy has not been subjected to randomized trials, but is widely accepted as a component of standard management. Table 1 describes the results of systematic reviews for five therapies used in the management of spasticity in patients with cognitive palsy. Those provided past the Cochrane Collaboration can be assessed at http://www.mrw.interscience.wiley.com/cochrane. For each of these therapies systematic reviews have provided evidence of benefit. Botulinum toxin type A for management of spasticity and casting for management of equinus deformity of the foot are probably the most widely available and used. Dorsal rhizotomy is a more than invasive approach to the direction of spastic diplegia and is reserved for the more difficult cases.
Table 1
Therapies used to manage spasticity in cognitive palsy
| Therapy | # studies (# patients studied) | # randomized trials (# patients randomized) | Conclusions |
|---|---|---|---|
| Botulinum toxin type A in the treatment of lower limb spasticity | 3 (52) | 3 (52) | no strong controlled evidence constitute to support or refute the use of Botulinum toxin type A for the treatment of leg spasticity (one) |
| Botulinum toxin type A for treatment of spastic equinus foot | Not provided | four (183) | Botulinum toxin type A superior to placebo for improvement of gait (2) |
| Botulinum toxin A as an adjunct to handling in the management of the upper limb in children with spastic cerebral palsy | 2 (44) | ii (44) | 1 of the two randomized trials reported promising results in support of reduced muscle tone following Botulinum toxin A injections; show not sufficient to support or refute the utilize of this therapy as an adjunct to managing the upper limb in children with spastic cognitive palsy (3) |
| selective' dorsal rhizotomy plus physiotherapy | 3 (90) | 3 (90) | selective' dorsal rhizotomy (SDR) plus physiotherapy reduces spasticity in children with spastic diplegia slightly improves gross motor part (iv) |
| casting for equinus | 21 (473) | ix (238) | No randomized trials available comparing protocols of casting in current use with no handling; no strong and consistent testify that combining casting and Botulinum toxin A is superior to using either intervention forth; no evidence that the order of these two treatments affects outcome (5) |
Other therapies to improve role in cerebral palsy are listed in Table 2. Therapies specific for hemiplegia, such as constraint-induced movement therapy (CIMT) and manus-arm bimanual intensive therapy (Habit), have been studied in a relatively small number of individuals. With CIMT, the non-involved upper extremity is restrained and the involved extremity is engaged in targeted do. With HABIT, structured tasks requiring bimanual function are skillful in the context of play and functional activities. While more written report is warranted, these announced to hold promise of benefit. More research on the effects of hyperbaric oxygen therapy is required, as in that location is considerable uncertainty about its efficiency and adverse furnishings, and this treatment costs approximately $400 per 90-minute session.
Table 2
Therapies used to improve part in children with cognitive palsy
| Therapy | # studies (# patients studied) | # randomized trials (# patients randomized) | Conclusions |
|---|---|---|---|
| Speech and language therapy to better the advice skills | 11 (46) | 1 (20) | trend towards improved communication skills; evidence not sufficient to recommend change in practice (1) |
| Constraint-induced movement therapy in the handling of the upper limb in children with hemiplegic cognitive palsy | iii (94) | 2 (49) | significant benefit in a unmarried trial; positive tendency favoring constraint-induced movement therapy (CIMT) and Forced Use; "given the limited testify, the utilize of CIMT, modified CIMT and Forced Utilize should exist considered experimental in children with hemiplegic cognitive palsy." (2) |
| Hyperbaric oxygen therapy | half dozen (449) | 2 (137) | Hyperbaric oxygen therapy and pressurized room air improved function to a similar caste; a proportion of patients treated with this therapy experience seizures (three) |
Prognosis
Equally discussed to a higher place, prognosis for independent ambulation depends in big function on the type of motor impairment. Airing status, intelligence quotient, quality of speech communication, and paw function together are predictive of employment status. For example, in a study of adults with cognitive palsy, intelligence quotient ≥ 80, and understandable speech, who were ambulatory and independent of the need for "meaning assistance", xc% were employed in a "competitive job" (i.e., one which could be filled by a similarly qualified person without a disability).
Mortality also is strongly associated with both the level of functional harm equally well as associated non-motor impairments. In ane report of over 2014 individuals with cognitive palsy, the strongest predictor of bloodshed was intellectual disability. For example, among those with profound intellectual inability (i.east., IQ < 20), but one half survived into adulthood; whereas among those with IQ > 35, 92% survived to adulthood. More by and large, mortality adventure increases incrementally with increasing number of impairments, including intellectual, limb function, hearing, and vision. In a recent population-based study, the shortest life expectancy was observed among those individuals who were unable to lift their head in decumbent, who had a life expectancy of 20 years.
Antenatal approaches to prevention
To an alarming extent, cerebral palsy is mistakenly attributed to acts of omission or commission by obstetricians. Among the most important lines of research during the by ii decades is the investigation of the role of perinatal infection and inflammation in caused brain damage in both term and preterm fetuses and newborns(7;xiv), and the role of prothrombotic factors and other causes of neonatal stroke in the pathogenesis of congenital hemiplegia(15). Although epidemiologic studies betoken that less than 10% of cerebral palsy results from intrapartum hypoxia, three quarters of United States obstetricians report beingness the field of study of a litigation upshot, most frequently related to their allegedly causing cerebral palsy by not preventing or treating fetal hypoxia(sixteen). In a report of 46 malpractice cases, investigators ended that "the severity of the patient'southward disability, not the occurrence of an adverse event or an adverse effect due to negligence, was predictive of payment to the plaintiff"(17).
Many assumptions about the effectiveness of obstetric care for preventing cognitive palsy generally are based on weak or no evidence(16). Published checklists provide a more than evidence-based arroyo to attribution(18;nineteen). A intrapartum outcome as a crusade of cognitive palsy is more probable if pregnant fetal acidosis (such as pH < seven.0) and neonatal encephalopathy are observed, and is more likely with spastic quadriplegia or dyskinetic cerebral palsy. While these events might be the event of intrapartum hypoxia, they might besides be the result of fetal infection. Thus in that location is virtually always considerable incertitude as to the cause of cerebral palsy, peculiarly among infants born at or well-nigh term.
Nonetheless, considering approximately i-half of all new cases of cerebral palsy ascend from the grouping of neonates born prematurely, it is possible that interventions which either prolong gestation or decrease the run a risk of preterm delivery will also decrease the risk of cerebral palsy. Specific approaches to reduce the rate of preterm birth, that are supported by a high level of prove, include limiting the number of embryos transferred with in vitro fertilization, smoking cessation during pregnancy, screening for and handling of asymptomatic bacteriuria during pregnancy, antiplatelet drugs to prevent preeclampsia, 17α-progesterone caproate, and cervical cerclage for women with previous preterm birth and short cervix (i.e., < ii.5 centimeters)(xx). In addition, interventions which have been shown to prolong pregnancy include calcium channel blockers and an oxytocin antagonist (atosiban) for women with preterm labor and erythromycin for women with premature rupture of the membranes(20). In addition to these measures, the results of a meta-analysis of four trials suggests that treatment of mothers expected to deliver before 36 weeks gestation with glucocorticoids (eg. β-methasone) reduces the risk of cerebral palsy. In the Australasian Collaborative Trial of Magnesium Sulphate, magnesium sulfate handling of mothers at risk for preterm birth before 30 weeks gestation reduced the risk of substantial gross motor dysfunction, and in a multicenter randomized trial in France a tendency towards a reduction in cerebral white matter damage was observed. More than information about the possible beneficial of antenatal magnesium sulfate is expected shortly from the National Institutes of Health Maternal Fetal Medicine Network trial (Benefits of Antenatal Magnesium Sulfate).
Postnatal approaches to prevention
Most term or near-term infants who develop cerebral palsy accept uneventful neonatal courses. A notable exception are those who have neonatal encephalopathy. One of the presumed causes of neonatal encephalopathy is intrapartum cerebral hypoxia and ischemia, which in severe cases could event in permanent brain harm manifesting as cognitive palsy. In such infants, hypothermia, either selectively applied to the head or total body, appears to decrease the chance of neurodevelopmental impairments, including cerebral palsy(5). While this intervention appears to be effective, it is applicable to only a small proportion of children who later on develop cerebral palsy.
In preterm infants, caffeine is the only therapy that has been shown in a multicenter trial to decrease the adventure of cerebral palsy. In this trial, extremely low birth weight infants were randomized to caffeine or placebo in the showtime days of life. While the results might use only to a small proportion of preterm infants, information technology is this subgroup that is at highest risk of cognitive palsy. Postnatal steroids, given to premature infants to decrease lung inflammation and subtract the run a risk of bronchopulmonary dysplasia, increase the run a risk of cerebral palsy. Thus limiting the utilise of this treatment can be expected to reduce the risk of cerebral palsy. The goal of recently completed trial by the National Institutes of Wellness Neonatal Research Network was to study the effect of aggressive phototherapy for hyperbilirubinemia on neurodevelopmental outcome. The results of this trial may be relevant to the prevention of cerebral palsy in extremely depression birth weight infants.
Summary
Cerebral palsy is relatively common cause of persistent motor impairment and is associated with a multifariousness of developmental disabilities. In developing countries, approximately 1 half of cases occur in prematurely born infants, and in this group the prevalence of cerebral palsy in developed countries appears to be decreasing over the by decade. In full term infants, the prevalence has been remarkably stable despite the advent of continuous fetal heart rate monitoring. The care of children with cognitive palsy requires a multidisciplinary, comprehensive, and coordinated approach. In developed countries, the self-reported quality of life for adolescents with cerebral palsy, except for severe cases, is similar to that of adolescents without cerebral palsy. Interventions that hold promise for reducing the prevalence of cerebral palsy include interventions to decrease the risk of premature birth, antenatal steroids given to mothers expected to deliver prematurely, treatment of mothers who are expected to evangelize prior to xxx weeks gestation with magnesium sulfate, hypothermia for neonates diagnosed with hypoxic-ischemic encephalopathy, and caffeine for extremely depression birth weight infants.
Footnotes
Sources of support: none to study
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Evaluation to See if My Baby Has Cerebral Palsy
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3051278/