Several risk factors of cerebral palsy have been identified, such as perinatal asphyxia. Although some such risk factors may be preventable, a general predictable method of preventing the disease is currently unknown. Some studies have indicated promising preventative measures, but their effects have not been extensively tested and are therefore chancy. However, the literature does point to techniques that may help prevent specific known corollaries of cerebral palsy, such as his displacement.
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PURPOSE OF REVIEW: To use evidence of good medical quality to update information on strategies for prevention of cerebral palsy, and on the success of these preventive efforts to date. RECENT FINDINGS: Causes of cerebral palsy, and therefore promising approaches to prevention, differ by gestational age group and by clinical subtype. Neuroimaging and neuropathology indicate the importance of white matter disorders and of ischemic stroke in cerebral palsy; birth asphyxia, congenital malformations, placental pathology, and genetic variants also contribute to cerebral palsy risk. Multiplicity of risk factors markedly increases risk. Recent studies indicate that mild hypothermia lessens cerebral palsy risk in term infants with moderate neonatal encephalopathy, and the possibility that administration of magnesium sulphate to women in preterm labor may aid in primary prevention of cerebral palsy in very preterm infants. SUMMARY: Past efforts to prevent cerebral palsy have not had the benefits sought, but recent results provide new hope and new challenges.
[Nelson, K. B. & Chang, T. (2008). Is cerebral palsy preventable? Current Opinions in Neurology, 21(2), 129-35.]
[ Abstract ]
The proposal by V. Vojta in 1974 to prevent development of cerebral palsy in "motor risk" infants by special treatment has been investigated in 11 Danish and 10 Swedish babies and compared with 30 control infants with similar risk, who were not given Vojta treatment. We found a tendency for "uncomplicated" cerebral palsy cases to accumulate in the control group, although the difference was non-significant on 1 5% level. Further controlled studies must be completed before it is possible to accept the prophylactive treatment of cerebral palsy recommended by Vojta.
[Brandt, S., Lonstrup, H. V., Marner, T., Rump, K. J., Selmar, P., Schack, L. K., d’Avignon, M., Noren, L. & Arman, T. (1980). Prevention of cerebral palsy in motor risk infants by treatment ad modum Vojta. A controlled study. Acta Paediatrica Scandinavica, 69(3), 283-6.]
[ Abstract ]
In 1994, a register for cerebral palsy and a health-care programme were started in southern Sweden with the aim of preventing dislocation of the hip in children with cerebral palsy. It involved all children with cerebral palsy born in 1992 or later. None of the 206 affected children born between 1992 and 1997 has developed a dislocation following the introduction of the prevention programme. Another 48 children moved into the area and none developed any further dislocation. Of the 251 children with cerebral palsy, aged between five and 11 years, living in the area on January 1, 2003, only two had a dislocated hip. One boy had moved into the area at age of nine with a dislocation and a girl whose parents chose not to participate in the programme developed bilateral dislocation. One boy, whose condition was considered to be too poor for preventative surgery, developed a painful dislocation of the hip at the age of five years and died three years later. Eight of 103 children in a control group, consisting of all children with cerebral palsy living in the area between 1994 and 2002, and born between 1990 and 1991, developed a dislocation of the hip before the age of six years. The decreased incidence of dislocation after the introduction of the prevention programme was significant (p < 0.001). Dislocation of the hip in cerebral palsy remains a serious problem, and prevention is important. Our screening programme and early intervention when lateral displacement of the femoral head was detected appear to be successful.
[Hagglund, G., Andersson, S., Duppe, H., Lauge-Pedersen, H., Nordmark, E. & Westbom, L. (2005). Prevention of dislocation of the hip in children with cerebral palsy. The first ten years of a population-based prevention programme. The Journal of Bone and Joint Surgery. British Volume, 87(1), 95-101.]
[ Abstract ]
OBJECTIVES: Intrapartum foetal monitoring goal is to prevent foetal asphyxia and its most severe consequence: cerebral palsy (CP). In this paper we describe the detection methods and the criteria needed to assess asphyxia during labour for preventing CP. Foetal cerebral damage assessment is considered from the medical-legal point of view. CP represents the most frequent pathology of childhood related to pregnancy and childbirth with an incidence of 0.2% in children born alive. It is clinically regarded as the result of a spectrum of diseases due to damage or to faded development of the nervous system which generally appears at the time of the first stage of intra-uterine growth or depends on problems arising at birth. The goal of our analysis is to recall the various moments in which this event can take place and, if possible, the moment and the degree of the event of asphyxia and its effect on foetal conditions, in order to control and treat it. STUDY DESIGN: One hundred and eighty-eight fetuses were evaluated by means of Apgar score, intrapartum cardiotocography, observation of the presence of meconium stained amniotic fluid, and clinical features of distress at birth. Lactate concentrations were measured during labour and at delivery in blood samples obtained from the foetal presenting part (foetal scalp) and from the umbilical cord with the use of a rapid electrochemical technique. RESULTS: Evidence of clinical foetal distress was not related to the severity of asphyxia. An increased lactate level was found in asphyctic infants and a clear correlation between lactic acidosis and foetal distress was documented. Low Apgar scores were observed in infants with moderate or severe asphyxia at delivery. Scalp lactate correlated significantly with umbilical artery lactate (P = 0.49, 0.01), but with neither Apgar score at 1 min (R = -0.21, ns) nor at 5 min (R = -0.11, ns). Lactate concentration was higher in case of instrumental delivery compared to spontaneous delivery (P = 0.0001). No perfect correlation was found between lactate level and neonatal outcome, but there were not a significant number of neonates with immediate complications. The rate of instrumental delivery in the distress group was significantly higher than in that of the healthy fetuses (P < 0.01), so spontaneous labour was less frequently associated with foetal distress than instrumental delivery (P < 0.01). In the distress group, severe variable decelerations were generally recorded in the second stage of labour. The incidence of neonatal Apgar score </=7 in neonates with abnormal baseline foetal heart rate (FHR) was higher than in those with severe variable decelerations, mild variable decelerations, and transient tachycardia (P < 0.05). The duration of the active second stage of labour correlated significantly with the presence of foetal lactate (P < 0.001) at the time of crowning of foetal head, and the presence of lactate in umbilical cord blood at delivery (P < 0.001). Expulsion time >/=45 min, compared with a shorter active second stage, and acidaemia at birth implied larger arterial-venous lactate differences (P < 0.001). The presence of foetal lactate at crowning was also significantly associated with the level of umbilical arterial-venous lactate difference (P = 0.03). CONCLUSIONS: Analysis of the fetus should start with the assessment of lactates and acid-base balance. The method which revolutionized the techniques of foetal monitoring is undoubtedly represented by cardiotocography. However, likely most of neurological outcomes are not correlated with a perinatal event or with peripartum asphyxia. Approximately 10% of cases of CP would actually be due to perinatal asphyxia, and this percentage approaches approximately to 15% if we consider only newborns at term. This again confirms the weak association of a causal relationship between asphyxia and CP. In addition, available foetal suffering markers are vague and allow to identify only less than half of the effective cases of newborns which will develop CP.
[Borruto, F., Comparetto, C. & Treisser, A. (2008). Prevention of cerebral palsy during labour: Role of foetal lactate. Archives of Gynecology and Obstetrics, 278(1), 17-22.]
[ Abstract ]
Birth asphyxia is a broad term that refers to intrapartum asphyxia sufficient to cause neurological damage in some newborns and, rarely, intrapartum or neonatal death. Cerebral palsy and long-term neurological complications such as learning difficulties and motor impairments may be due to causes other than birth asphyxia. Several intrapartum events may cause asphyxia (i.e. hypoxia and metabolic acidosis) leading to the likelihood of neurological injury. The cardiotocograph (CTG) is a screening tool that is used to assess fetal well-being during labour and to identify the possibility of asphyxia. Abnormality of the CTG, sometimes severe enough to be described as a pathological trace, is commonly termed 'fetal distress', although many fetuses with such traces may not have hypoxia and metabolic acidosis. In current practice, the events are appropriately termed 'pathological CTG trace' or 'acidotic pH' rather than 'fetal distress'. Accurate interpretation of CTG is essential, and it is important to recognize a fetus that shows a pathological CTG in labour that may imply possible hypoxia and birth asphyxia. Considering the wider clinical picture in interpreting the CTG, and taking timely and appropriate action based on the findings, may help prevent birth asphyxia.
[Chandraharan, E. & Arulkumaran, S. (2007). Prevention of birth asphyxia: Responding appropriately to cardiotocograph (CTG) traces. Best Practice & Research: Clinical Obstetrics & Gynaecology, 21(4), 609-24.]
[ Abstract ]
Background. The purpose of this article is to present treatment outcomes for dysplastic hips in cerebral palsy, operated by tenotomy of the thigh adductor muscles and the greater iliopsoas muscle. Material and methods. 40 dysplastic hips in 20 severely tetraplegic cerebral palsied children were evaluated. The study group included children from 4 to 8 years. All patients were examined radiologically, with X-rays taken in anterio-posterior position and measurements were taken to record migration percentage according to Reimers. On that basic the hips were evaluated and the risk of possible paralytic hip luxation was predicted. In all the assessed patients prophylactic tenotomies of adductors and psoas muscles were made. The follow-up period was 1 year. Results. In 18 patients we observed better hip stability and decreased migration percentage in the evaluated hips. In two patients (four hips) we observed no changes of migration percentage. No deterioration of hip functions was observed in there joints.
[Potasz, P. & Dobrowolski, J. M. (2002). Surgical prevention of hip luxation in cerebral palsied children. Ortopedia, Traumatologia, Rehabilitacja, 4(1), 8-10.]
[ Abstract ]
OBJECTIVE: To compare neurodevelopmental outcome of survivors of the multicentre trial of etamsylate (the iRNN for ethamsylate) for prevention of periventricular haemorrhage in very low birthweight infants. DESIGN: Double blind, single observer, prospective follow up of placebo controlled study. SETTING: Six neonatal intensive care units in the United Kingdom. Neurodevelopmental outcome was assessed in health premises or children's homes. SUBJECTS: 268 of 276 survivors of the original study were seen between 3.5 and 4.2 years of age. All were inborn and weighed 1500 g or less at birth. INTERVENTION: Etamsylate 12.5 mg/kg or placebo six hourly from within one hour of delivery for four days. MAIN OUTCOME MEASURES: McCarthy scales of children's abilities, standardised neurological examination, full physical examination, functional assessment, seven letter Stycar vision test, and audiometry. RESULTS: There was no difference between the groups in neuromotor outcome (cerebral palsy) or in the general cognitive index (GCI) of the McCarthy scales (mean GCI was 93.3 for the etamsylate group (n = 133) and 89.7 for the placebo group (n = 131); p = 0.10). There were more children with GCI < 70 (9 v 19; p = 0.047) or </= 50 (3 v 11; p = 0.03) in the placebo group. Fewer children in the etamsylate group had squints (17 v 30; p = 0.042) or required surgery for patent ductus arteriosus (1 v 8; p = 0.036). CONCLUSIONS: Etamsylate was not associated with a reduction in cerebral palsy. Severe cognitive impairment was reduced, but more children died and the improvement may be because fewer survived with low GCI.
[Schulte, J., Osborne, J., Benson, J. W., Cooke, R., Drayton, M., Murphy, J., Rennie, J. & Speidel, B. (2005). Developmental outcome of the use of etamsylate for prevention of preiventricular haemorrhage in a randomised controlled trial. Archives of Disease in Childhood. Fetal and Neonatal Edition, 90(1), F31-5.]
[ Abstract ]
The effectiveness of ethamsylate in the prevention of periventricular haemorrhage (PVH) in very low birthweight infants was evaluated by means of a multicentre, placebo-controlled, double-blind trial. In 330 infants without evidence of PVH on initial cranial ultrasound examination there was little difference between ethamsylate and placebo groups with respect to subependymal haemorrhage, but intraventricular and parenchymal haemorrhages developed in 30/162 infants (18.5%) in the treated group, compared with 50/168 (29.8%) in the control group (p less than 0.02). The incidence of intraventricular and parenchymal haemorrhage in survivors was 20/137 (14.6%) in the ethamsylate group and 37/146 (25.3%) in the controls (p less than 0.05). In 30 infants with evidence of PVH on the initial scan, ethamsylate treatment seemed to limit parenchymal extension. Analysis of the total cohort of 360 infants showed that the proportion of infants in whom an increase of two or more grades of severity of PVH was recorded during the trial was lower in the treated than in the placebo group (p less than 0.01). No adverse effects were attributed to ethamsylate therapy. The reported incidence of patent ductus arterious was lower in the treated than in the placebo group (p less than 0.02). Mortality was similar in the two groups.
[Benson, J. W., Drayton, M. R., Hayward, C., Murphy, J. F., Osborne, J. P., Rennie, J. M., Schulte, J. F., Speidel, B. D. & Cooke, R. W. (1986). Multicentre trial of ethamsylate for prevention of periventricular haemorrhage in very low birthweight infants. Lancet, 2(8519), 1297-300.]
[ Abstract ]
Intrapartum fetal health surveillance, in particular electronic fetal heart-rate monitoring (EFM), is a perinatal issue that has sparked much debate both nationally and internationally. Prevention of cerebral palsy is a major objective of all health-care providers when assessing fetal health in labour. The Fetal Health Surveillance Working Group of the Society of Obstetricians and Gynaecologists of Canada (SOGC) should be commended for its efforts in presenting and discussing the literature and for raising important issues in EFM in the SOGC's Clinical Practice Guideline on Standard Fetal Surveillance in Labour, published in JOGC in March 2002, the first half of the SOGC document Fetal Health Surveillance in Labour. These, as all, SOGC Clinical Practice Guidelines are widely used by hospitals and health-care providers when evaluating practices in their own environments, and we believe, as practitioners of and investigators in fetal health surveillance, that there is not good supporting evidence for recommending continuous intrapartum EFM for pregnancies in which there is an increased risk of perinatal death, cerebral palsy, or neonatal encephalopathy, or when oxytocin is being used for induction of labour, and that if we recommend that the fetal heart be electronically monitored while the nurse is elsewhere, we are on a slippery slope. We encourage reopening discussion regarding these recommendations in the document.
[Natale, R. & Dodman, N. (2003). Birth can be a hazardous journey: Electronic fetal monitoring does not help. Journal of Obstetrics and Gynaecology Canada: JOGC, 25(12), 10007-9.]
[ Abstract ]
CONTEXT: Prenatal magnesium sulfate may reduce the risk of cerebral palsy or death in very preterm infants. OBJECTIVE: To determine the effectiveness of magnesium sulfate given for neuroprotection to women at risk of preterm birth before 30 weeks' gestation in preventing pediatric mortality and cerebral palsy. DESIGN, SETTING, AND PATIENTS: Randomized controlled trial at 16 tertiary hospitals in Australia and New Zealand with stratification by center and multiple pregnancy. A total of 1062 women with fetuses younger than 30 weeks' gestation for whom birth was planned or expected within 24 hours were enrolled from February 1996 to September 2000 with follow-up of surviving children at a corrected age of 2 years. INTERVENTIONS: Women were randomly assigned to receive a loading infusion of 8 mL (4 g [16 mmol] of 0.5 g/mL of magnesium sulfate solution or isotonic sodium chloride solution [0.9%]) for 20 minutes followed by a maintenance infusion of 2 mL/h for up to 24 hours. MAIN OUTCOME MEASURES: Rates of total pediatric mortality, cerebral palsy, and the combined outcome of death or cerebral palsy at a corrected age of 2 years. RESULTS: Data were analyzed for 1047 (99%) 2-year survivors. Total pediatric mortality (13.8% vs 17.1%; relative risk [RR], 0.83; 95% confidence interval [CI], 0.64-1.09), cerebral palsy in survivors (6.8% vs 8.2%; RR, 0.83; 95% CI, 0.54-1.27), and combined death or cerebral palsy (19.8% vs 24.0%; RR, 0.83; 95% CI, 0.66-1.03) were less frequent for infants exposed to magnesium sulfate, but none of the differences were statistically significant. Substantial gross motor dysfunction (3.4% vs 6.6%; RR, 0.51; 95% CI, 0.29-0.91) and combined death or substantial gross motor dysfunction (17.0% vs 22.7%; RR, 0.75; 95% CI, 0.59-0.96) were significantly reduced in the magnesium group. CONCLUSIONS: Magnesium sulfate given to women immediately before very preterm birth may improve important pediatric outcomes. No serious harmful effects were seen.
[Crowther, C. A., Hiller, J. E., Doyle, L. W., Haslam, R. R., Australasian Collaborative Trial of Magnesium Sulphate (ACTOMgSO4) Collaborative Group. (2003). Effect of magnesium sulphate given for neuroprotection before preterm birth: A randomized controlled trial. JAMA: The Journal of the America Medical Association, 290(20), 2669-76.]
[ Abstract ]
This article reviews clinical and experimental evidence as to whether magnesium sulfate, administered soon before premature birth, can reduce the high rate of cerebral palsy in tiny infants. Three observational studies have reported an association of magnesium sulfate with lower rate of cerebral palsy, whether treatment was for maternal preeclampsia or for tocolysis. One of these studies also noted a significant reduction in cognitive disability. In another study, no significant protective effect was seen except in a small subset of infants. Magnesium was neuroprotective in many but not all of a variety of experimental studies and has a variety of biologic effects that might account for benefit. All existing clinical studies had relatively small numbers of very premature infants. Although all attempted to control for possible confounders, such studies cannot provide definitive answers as to possible benefits or risks of magnesium therapy. Only randomized clinical trials are likely to resolve the question of whether a brief exposure to an agent which, in the American experience, is considered safe if administered with appropriate supervision, can reduce longterm neurologic disability in premature infants.
[Hirtz, D. G. & Nelson, K. (1998). Magnesium sulphate and cerebral palsy in premature infants. Current Opinions in Pediatrics, 10(2), 131-7.]
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The hereditary spastic mouse was studied as a model of cerebral palsy in childhood to test the hypothesis that intramuscular botulinum toxin A would prevent the development of calf-muscle contractures. A prospective randomised controlled trial of calf injection with botulinum A compared with injection of normal saline was performed on juvenile mice. At maturity, the calf muscles of the spastic mice were 16 per cent shorter than those of their normal siblings. The calf muscles of spastic mice injected with botulinum toxin A grew to within 2 per cent of normal length. This difference in mature muscle length was highly significant.
[Cosgrove, A. P. & Graham, H. K. (1994). Botulinum toxin A prevents the development of contractures in the hereditary spastic mouse. Developmental Medicine and Child Neurology, 36(5), 379-85.]
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