# Introduction illiam John Little in 1862, an Orthopaedic Surgeon presented a group of Children with tonal and developmental abnormalities, which he described as spastic rigidity. (1) Many of these children had a history of prolonged labour, preterm delivery. Because of frequency of these perinatal problems, Little postulated that the motor defects resulted directly from difficulties in the birth process. This opinion was widely held for over a century. Yet there were early critics, chief among them Sigmund Freud, who speculated that, perinatal difficulties were the result of pre exisisting abnormalities in the foetus rather than the cause of cerebral palsy. (2) This study was undertaken to identify and quantitate the major causes of cerebral palsy. The analysis were based on specific disorders that might damage a child's brain. (3) The most widely discussed of these disorders is birth asphyxia, with some people claiming that it is a frequent and others could be misleading because it is possible that such disorders are being missed or that insufficient cases have been analysed to find a correlation between them and cerebral palsy. (4) The first goal of the present study was to determine how much of a role birth asphyxia has in the genesis of cerebral palsy. A second goal was to quantitate the roles of chronic antenatal hypoxia disorders, congenital disorders, hypoglycemia, oxytocin, toxaemia of pregnancy, mal presentations and other prenatal factors as causes of cerebral palsy. (5) II. natal clinic and who is attending the delivery. The same was collected back to us by above mentioned institutes on a fixed date of every month, at the time of monthly review meeting at District head quarter with district Civil Surgeon. Thus from 1 st Feb 1998 to 31 st Jan 2000, a prospective study of 31,804 antenatal mothers were followed up till delivery and 30,080 live births were observed in Sindhudurg district. The total number of live births for the above mentioned period was 32366 as per the vital statistics department of District Health Officer, Sindhudurg, thus un accounting the total live births of 2286, which include deliveries in small dispensaries, other nursing homes of outside the districts and home deliveries. All the children born were seen and examined at every six months intervals to identify cerebral palsy by a systematic and uniform record keeping system. The last neurological examination in the study was conducted in February 2002. Data received from above mentioned institute enlisted for investigation, which became available for analysis in March 2002. Data for antenatal mothers and intranatal mothers compiled by the respective doctors in the stringent protocols updated, we are fairly confident that the protocol data accurately reflect the Cerebral palsy pattern in Sindhudurg district. 1065 children could not be analysed because the mothers delivered at different hospitals other than above mentioned institutes. # Material & Methods # III. # Results Analysis were undertaken in a prospective study of 31,804 ante natal mothers who delivered from 1 st Feb 1998 to 31 st Jan 2000.. 246 children were identified as cerebral palsy in 30,080 live births at the end of 3 rd serial examination. Thus 33% (82/246) victims of Cerebral palsy had birth asphyxia the presumed cause of their cerebral palsy. Of this 26% (64/246) were cases of quadriplegic cerebral palsy and 7% (18/246) non quadriplegic, which was attributable to the birth asphyxia. There was quiet a significant association of cerebral palsy with chronic antenatal hypoxic disorders.. Congenital disorders explained about one third of quadriplegic cerebral palsy. Birth asphyxia was not a significant antecedent of non quadriplegic cerebral palsy. Finally the findings of the present study under score the importance of making accurate measurements and observations on neonates to avoid mistakes attributing non asphyxial cerebral palsy to birth asphyxia. The overall incidence of cerebral palsy for Sindhudurg Dist. amount to 8.1 per thousand live births over a period of 1998 to 2000. # IV. # Discussion Most studies that have attempted to determine if birth asphyxia is a cause of cerebral palsy, have used low Apgar scores and foetal distress to identify asphyxia. Low Apgar scores and foetal distress are often non hypoxic in origin, so their use as indicators of birth asphyxia could misattribute some non asphyxial cerebral palsy to asphyxia. (6) We explored this possibility by seeing how many victims of cerebral palsy who had low Apgar scores had a non asphyxial disorder as the basis for their cerebral palsy. During the past two decades, dramatic changes in obstetrical and perinatal care have included the increasing availability of foetal heart monitoring and foetal ultrasonography, the establishment of neonatal intensive care units, and the implementation of policies to encourage the regionalization of care and the transport of mothers carrying high-risk foetuses before delivery. If the occurrence of cerebral palsy reflected sub optimal obstetrical care, (6) then its prevalence would be expected to decline in response to these remarkable improvements in care, but it has not done so. (8) In an attempt to evaluate the relative contribution of all pregnancy-related factors, some epidemiologists have created analytic models that evaluate later events (for example, those occurring during the delivery) (9) in the light of earlier events (characteristics of the mother before pregnancy, firsttrimester events, and so on). (10) , in the victims of cerebral palsy, characteristic consequences of birth asphyxia were more often the result of non-asphyxial disorders. (11) These included muconium in the amniotic fluid, low 10 minute Apgar scores. Another perspective is gained by looking at the relative risks of various risk factors for cerebral palsy. Birth asphyxia had the highest relative risk for quadriplegic cerebral palsy. However, the low frequency of birth asphyxia in the population as a whole (82 of 30804) gave birth asphyxia a much smaller role as a cause of quadriplegic cerebral palsy. Difference in distribution of factors related to cerebral palsy is highly significant. Since these factors are not mutually exclusive i.e. same case of cerebral palsy can have more than one factor hence chi square test won't make any sense really. A child whose mother has long intervals between menses appears to be at increased risk for cerebral palsy. (12) The risk is increased if there has been an unusually short interval (less than three months) or an unusually long interval (more than three years) since the previous pregnancy. (13) In addition, mothers of children with cerebral palsy are more likely than other mothers to have a history of spontaneous abortion and stillbirth. These findings indicate that maternal menstrual and obstetrical factors convey information about the risk of cerebral palsy. Twins are more likely than singletons to have antenatal peri ventricular leukomalacia (14) and cerebral palsy. (15) Some of the increased risk of cerebral palsy among twins probably results from their gestational age and intrauterine growth retardation. In one study, an increase in the cesarean-section rate in the delivery of twins was not associated with a reduction in the prevalence of cerebral palsy. (16) The greater concordance for cerebral palsy among monozygotic than dizygotic twins also suggests a genetic basis, but it is compatible with placental problems that are unique to monozygotic twins as well. Mothers known to have been hyperthyroid or who were prescribed thyroid hormones or estrogen in pregnancy have been found to be at increased risk of giving birth to a child in whom cerebral palsy later develops. Non-vertex and face presentations of the foetus are associated with an increased risk of cerebral palsy. (17) One interpretation of this fact is that an abnormal presentation does not cause cerebral palsy, but rather may be a marker of preexisting difficulties. According to this hypothesis, foetuses with hypotonia and other abnormalities that will later be manifested as cerebral palsy are less able than others to move into a vertex position. The rate of cerebral palsy is 25 to 31 times higher among infants who weigh less than 1500 g at birth than among full-sized newborns. (18) Babies whose birth weight is less than 2500 g account for about one third of all babies who later have signs of cerebral palsy. (19) As a generalization, the lower the birth weight and the gestational age, the higher the risk of cerebral palsy (20) and peri ventricular leukomalacia. Thus it should not be surprising that a number of low birth weight and early gestational age children are associated with peri ventricular leukomalacia, even among babies born prematurely. (21) Nelson and Ellen berg wrote in 1986 "Of the . . . mother-infant pairs in the 5 percent with the highest risk (for cerebral palsy) only 208 percent produced a child with cerebral palsy, the false positive rate was thus 97 percent." Epidemiological studies published since then have not provided any reasons to change the impression that our ability to identify modifiable presumed causes of cerebral palsy is limited. The burden imposed by cerebral palsy on society has not abated despite recent advances in medical care. Indeed, the increased survival of preterm newborns at risk for the disease has resulted in an increased number of children with cerebral palsy, mainly of the spastic diplegic variety. (22) ![Volume XIV Issue IV Version I© 2014 Global Journals Inc. (US)](image-2.png "W") 1Sr. No.FactorNoIncidenceRelative Risk1Prematurity148/24660.2%54.42Low birth weight136/24655.3%52.23Low Apgar score & abnormal foetal heart rate86/24634.9%10.74IUGR on USG82/24633%15.15History of spontaneous abortion & stillbirth68/24627.06%5.76Toxaemia of pregnancy44/24617.9%8.17Forceps application42/24617%42.28Muconium stained liquor36/24614.7%1.29Malpresentation34/24613.9%8.610Oxytocin drip during labour26/24610.7%2.511Unusually long or short interval between pregnancy26/24610.6 %1.912Caesarian section16/2466.5%0.7813History of taking thyroid / oestrogen hormones16/2466.5%43.514Vaccum application12/2464.9%29.615Post maturity12/2464.9%1.616Bleeding during 1st , 2nd, 3rd, trimester of pregnancy8/2463.3%1.3The following positive antenatal, intranatalabortion and still births were detected in 27.6% (68/246).findings noticed are suggestive of quite a significantToxaemia of pregnancy was noted in 17.9% (44/246)association of cerebral palsy with chronic antenatalante natal mothers. Forceps were applied duringhypoxia disorders.deliveries in 17% (42/246). Muconium stained liquor60.2% (148/246) were born prematurely beforeduring labour was seen in 14.7% (36/246). Mal32 weeks of pregnancy. 55.3% (136/246) were low birthpresentations were seen in 13.9% (34/246). Oxytocinweight babies (below 2500 grams). Low Apgar scores &drip was started during labour in 10.6% (26/246). Anabnormal foetal heart rate during labour were present inunusually long or short interval between the pregnancy34.9% (86/246). Evidence of IUGR on USG waswas seen in ante natal mothers cerebral palsy childrendiagnosed in 33% (82/246). History of spontaneous10.6% (26/246). Caesarean section was performed in 2Sr. No.OE(O-F) 2 /E113649.5151.1214849.5196.032649.511.146849.56.953449.54.861249.528.478649.526.983649.53.691649.522.610849.534.7114449.50.6128249.521.3134249.51.1141249.528.4151649.522.6162649.511.1571.2EX = 792 x == 49.5 X 2 = 571.2, df = 15 p<0.001b) Difference is highly significant statistically Thus, efforts to prevent cerebral palsy will require a focus on factors and events during pregnancy including those that predispose the mother and foetus to preterm delivery and low birth weight. * On the influence of abnormal parturition, difficult labors, premature birth and asphyxia neonatorum, on the mental and physical condition of the child especially in relation to deformities WJLittle Transactions of the Obstetric Society of London 3 * SFreud Infantile cerebral paralysis Russin, Trans). Coral Gables 1897. 1968 FL University of Miami Press * Presented a paper on Incidence and risk factors contributing to the development of cerebral palsy -a prospective study of 30804 antenatal mothers RSKulkarni 22 Dec. 2001 At 46th Annual Conference of Indian Orthopaedic Association * How much of a role birth asphyxia and chronic antenatal hypoxia disorders have in the genesis of Cerebral Palsy? at 1st Annual conference of K RSKulkarni .K.M.S. of I.A.P.S.M Govt. RCSM Medical College Kolhapur on 1st August 2004 Presented a paper on * How much of a role birth asphyxia and chronic antenatal hypoxia disorders have in the genesis of Cerebral Palsy RSKulkarni At Asia Pacific Childhood Disability Update 2005 at Mumbai, on 4th December 2005 Presented a paper on * Trends in perinatal mortality and cerebral palsy in Westerm Australia LStanley Fj Watson Br. 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Project JKGrether SKCummins KBNelson Paediatr Perinat Epidemiol 6 1992 * Antenatal origin of neurologic damage in newborn infants. I Preterm infants MBejar R Wozniak P Allard Am J Obstet Gynecol 1988 * Rydhstrom H Prognosis for twins with birth weight less than 1500 gm the impact of cesarean sction in relation to fetal presentation Am J Obstet Gynecol 163 1990 * Etiologic factors in cerebral palsy NPaneth Pediatr Ann 15 191 1986. 194-5, 197-201 * Cerebral palsy in very low birthweight infants RWCooke Arch Dis Child 65 1990 * Survival and cerebral palsy in low birthweight infants: implications for perinatal care FJStanley Paediatr Perinat Epidemiol 6 1992 * Cooke RW Effects of birth weight gestational age, and maternal obstetric history on birth prevalence of cerebral palsy EBlair POStanley Fj ; Pharoah TCooke LRosenbloom Arch Dis Child 62 1987 Intrauterine growth and spastic cerebral palsy I. 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