|Year : 2015 | Volume
| Issue : 2 | Page : 108-113
Clinical profile, predisposing factors, and associated co-morbidities of children with cerebral palsy in South India
Vykuntaraju K Gowda1, Anil Kumar2, Sanjay K Shivappa2, Praveen Kumar Srikanteswara3, Shivananda2, MS Mahadeviah2, M Govindraj2, Premalatha Ramaswamy2
1 Department of Pediatrics Neurology, Indira Gandhi Institute of Child Health, Bengaluru, Karnataka, India
2 Department of Pediatrics, Indira Gandhi Institute of Child Health, Bengaluru, Karnataka, India
3 Department of Neurology, Bangalore Medical College and Research Institute, Bengaluru, Karnataka, India
|Date of Web Publication||22-Jun-2015|
Vykuntaraju K Gowda
Bangalore Child Neurology and Rehabilitation Center, HANS Complex, 8/A 1st Main 1st Cross, Manuvana, Near Adhichunchanagiri Choultry, Vijayanagar, Bengaluru - 560 040, Karnataka
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Introduction: Cerebral palsy (CP) is the most common physical disorder of children. Causes like jaundice and birth injury though are decreasing; complications resulting from the survival of low birth weight babies are replacing some of the older etiologies. Hence, this study was planned. Objectives: The objective was to study the clinical patterns, predisposing factors, and co-morbidities in children with CP. Materials and Methods: The present study is a hospital based prospective study conducted from January 2012 to January 2013 in children presenting to neurodevelopmental clinic at a tertiary care teaching hospital in India. Hundred cases with clinical features suggestive of CP were included in the study. Cases were evaluated by history, clinical examination, and necessary investigations. Results: Results of the study showed 81% of spastic, 12% of hypotonic, 5% of dystonic, and 2% of mixed CP cases. The mean age of presentation was 2 year, 2 month, and male to female ratio of 1:2. Pregnancy-induced hypertension (PIH) was the most common antenatal complication observed in 6%. Four percent had neonatal sepsis and 19% were born premature. Associated co-morbidities were mental retardation (55%), seizure disorder (46%), visual problems (26%), hearing problems (19%), and failure to thrive (47%). Discussion: Sex distribution observed in our study was male to female ratio of 1.2, which was comparable with a multicenter study in Europe. PIH was observed in 6% of cases, which was comparable with prior studies. Birth asphyxia was observed in 43% of cases. Eighty-one percent of the cases constituted a spastic variety of CP which was comparable to other studies. Conclusion: Perinatal asphyxia was the important etiological factor. We found preventable intranatal causes (60%) and antenatal causes (20%) forming a significant proportion. Co-morbidities were significantly observed in our study.
Keywords: Cerebral palsy, clinical profile, co-morbidities, predisposing factors, South India
|How to cite this article:|
Gowda VK, Kumar A, Shivappa SK, Srikanteswara PK, Shivananda, Mahadeviah M S, Govindraj M, Ramaswamy P. Clinical profile, predisposing factors, and associated co-morbidities of children with cerebral palsy in South India. J Pediatr Neurosci 2015;10:108-13
|How to cite this URL:|
Gowda VK, Kumar A, Shivappa SK, Srikanteswara PK, Shivananda, Mahadeviah M S, Govindraj M, Ramaswamy P. Clinical profile, predisposing factors, and associated co-morbidities of children with cerebral palsy in South India. J Pediatr Neurosci [serial online] 2015 [cited 2019 Oct 17];10:108-13. Available from: http://www.pediatricneurosciences.com/text.asp?2015/10/2/108/159191
| Introduction|| |
The developmental disabilities are a group of disorders differentiated by the pattern of delay among the developmental streams. The four streams of development include language, problem solving, motor, and social. Cerebral palsy (CP) is a disorder of development in which motor function abnormalities are the key features. It is the most common physical disorder in children first described by William John Little in 1861.
Cerebral palsy describes a group of permanent disorders of the development of movement and posture, causing activity limitations that are attributed to nonprogressive disturbances that occurred in the developing fetal or infant brain. The motor disorders of CP are often accompanied by disturbances of sensation, perception, cognition, communication, behavior, epilepsy, and by secondary musculoskeletal problems. ,,,,,,,,, The definition and classification of CP, April 2006 document is offered for international consensus and adoption, with the intent of providing a broad spectrum of audience with a common conceptualization about CP. 
Because of the wide variety of causes of CP, the exact numbers from different studies do not completely match. However, there is a remarkable similarity in the prevalence across the world, from Sweden in the 1980s with a prevalence of 2.4 per 1000  and 2.5 per 1000 in the early 1990s,  2.4 per 1000 from Malta,  2.5 per 1000 from Finland,  and 1.6 per 1000 in China.  Considering the difficulty in making a specific diagnosis, and especially finding mild cases, these numbers probably reflect much more variation in counting than clear differences in prevalence.
Ravn et al. reported the total CP birth prevalence has been significantly decreasing since the birth period 1983-1986 with 3.0 per 1000 live births until the period 1995-1998 with 2.1 per 1000 live births. The overall decrease was seen in preterm infants (<31 weeks) as well as in term infants and despite a simultaneous fall in perinatal and early neonatal mortality in the preterm group. Analyzing the subtypes of CP we found a significant increase in the numbers as well as the rate of unilateral CP with a simultaneous fall in the numbers as well as the rate of bilateral CP. 
Cerebral palsy prevalence is remarkably similar in developed countries. Nineteen of the 27 reports show prevalence between 1.5 and 2.5 per 1000 live births or child survivors, and all studies show prevalence between 1.2 and 3.0 per 1000 live births.  For CP at all birth weights, the overall impression is stability over time, but with a slight increase in prevalence in the 1980s. There is a suggestion that this increase may be on the decline. CP prevalence per 1000 live born infants who weigh <1500 g exhibited a sharp increase in the 1980s which seems to be on the decline. A similar, but slightly less pronounced trend was found in infants who weigh between 1500 g and 2499 g. The time trend for infants who weigh more than 2500 g shows an up-and-down pattern with no obvious trend.  It also is apparent that the slight increase in CP prevalence that is seen in all infants reflects the increase in CP in very low birth weight (VLBW) infants, which is entirely a consequence of their increasing survival. The decline in CP in such infants recently may reflect improvements in care of VLBW infants that are beginning to affect rates of CP or it simply may be sample variance, only time will tell. 
Causes like jaundice and birth injury are decreasing and on the other hand complications resulting from the survival of more low birth weight (LBW) babies are replacing some of the older etiologies. Prematurity and the factors responsible for the same, natal causes like intra-partum asphyxia, birth injury and the factors responsible for those, postnatal causes like infections, kernicterus, and other metabolic impairments constitute preventable etiologies of CP. If we are able to reduce the incidence of CP in future, the area's most amenable to intervention are those related to preventing postnatal brain injury in infants and those reducing preterm births. The present study intends to look into the present spectrum, etiology, risk factors, and co-morbidities of CP.
| Materials and Methods|| |
All children presenting with clinical features suggestive of CP to the neurodevelopmental clinic at Indira Gandhi Institute of Child Health over a period of 1-year (January 2012 to January 2013) were enrolled. History and a clinical examination using systematically designed forms were taken. MRI of brain was done to find out the cause and severity of brain injury. Intelligent quotient and associated behavioral problems like autistic features, hyperactivity was done by a clinical psychologist. Visual evaluation was done by a pediatric ophthalmologist and visual evoked potentials. Hearing assessment was done by an audiologist with brain stem auditory evoked potentials. Electroencephalogram was done to detect convulsions in children with a history of epilepsy. Following c ases were included: Cases of developmental delay with neurological examination consistent with CP; nonprogressive brain malfunction manifested early in life. Progressive neurological disorders were excluded.
| Results|| |
Our study group composed of 100 cases. Age of presentation at the first diagnosis was <1-year (28%), 1-4 year (65%), 5-10 year (6%), and more than 10 year (1%) [Table 1]. Male to female ratio of 1.2:1 was noted. Fifty percent were each from urban and rural regions. Distribution of cases as per socio-economic status (as per modified Kuppuswamy classification) observed was upper-middle - 11%, lower middle - 53%, upper lower - 36%. Common age of mother at birth of affected children was 19-25 year (72%) [Table 1]. Sixty-four percent of children were born to nonconsanguineous and 36% to consanguineously married couples (32% second degree and 4% third degree). Similar history of CP in family was observed in 5 cases (1 case with cerebral malformation, 2 cases secondary to prematurity, and two cases of perinatal asphyxia).
Birth order and gestational age of the affected children are shown in [Table 1]. Prematurity was a predominant finding (50%) in spastic diplegia. Extreme prematurity was observed in dystonic CP (severe form). Birth weights of the affected children are shown in [Table 1]. Extremely LBW was observed in cases of spastic diplegia. LBW was observed in 30% of our cases.
Antenatal complications observed are depicted in [Table 1]. The modes of delivery observed in our study were: Vaginal delivery (81%), instrumentation (3%), caesarean section (12% - the indications being: 3 cases of transverse lie, 9 cases of nonprogression of labor). The places of delivery observed were: Institutional 94% (primary health center - 46%, referral [secondary/tertiary center] - 48%), home - 6%. Forty percent of them required resuscitation at birth. No data about APGAR score is available in our study. Postnatal complications observed in our study are shown in [Table 1].
Various risk factors observed in our study are shown in [Table 2]. Encephalopathy after birth was observed in 49% of bilateral spastic CP cases. Genetic causes or malformations were observed in 50% of hypotonic CP cases. Classifications of CP and the associated problems are shown [Table 2].
| Discussion|| |
The mean age of presentation of CP cases observed in our study was 2 year and 2 month and the median age of presentation was 2 years. More severe forms of CP presented earlier and an exception being dystonic CP in our study, and that might be as a result of small number of dystonic CP seen in our study. The presenting age in our study was when concerns regarding standing, walking, talking, and communication were at their peak. Sex distribution observed in our study was male to female ratio of 1.2 which was comparable with a multicenter study in Europe (2002) in which male to female ratio of 1.33 was observed.  No sex predisposition was seen. Consanguinity was observed in 36% of our cases which was comparable with few Turkish studies who have noted a high number of marriages between relatives (21% of all marriages). , The increased frequency of consanguinity among parents of children with CP, and the strong association with a positive family history suggests the role of genetic factors in the pathogenesis of CP in this environment. 
Region of distribution of cases was equal among urban and rural population. In urban scenario, increasing antenatal risk factors and increased morbidity secondary to improved neonatal care were significant, whereas inadequacy of efficient obstetric care was the risk factor observed in the rural scenario.
In our study, socio-economic status of the study population was 53% Class III and 36% Class IV as per modified Kuppuswamy classification. A population-based study in Ireland  reported a significantly higher risk of CP, particularly diplegia, among children born to families of unskilled manual workers. We did not observe a significant correlation with socioeconomic status and diplegia in our study.
Birth order of the affected child in our study showed 65% being first born and 23% were second born which was comparable to previous studies. , Incidence of CP was less in higher order birth because of improved knowledge, attitude, and practice of parents in seeking obstetric and perinatal care.
History of CP in the family was observed in 5% of cases in our study. It was 2.5% in Sharma et al.,  and 2% in Hughes and Newton study.  Higher incidence observed in our study might be because of the high incidence of consanguinity observed in our study.
Gestational age of the affected children observed in our study was term gestation in 81%, late preterm (34-36 week) in 4% and preterm (<34 week) in 15%. Six out of the 19 preterms (32%) had spastic diplegia. Periventricular leukomalacia is most commonly observed in prematurity. Dystonic CP was observed in extreme prematurity (<28 week), as they are susceptible for global ischemia. LBW was observed in 30% of our cases, but prematurity was seen in 19% indicating that 11% of term children were intrauterine growth retardation in our study. Prior studies have noted that diplegia is the dominant type of CP (39.8%) and most of those cases (71.6%) were preterm. Children with spastic diplegia are almost universally appropriate for gestational age. , In agreement with few prior studies,  suggesting a relation between tetraplegic phenomena and small-for-gestational age term infants, 72.9% of cases of tetraplegia in a Turkish study were seen in term infants of whom 66% were small for gestational age. 
In terms of the type of CP, a prior study found that the spastic type of CP was the predominant form in preterm and term infants.  In our study also, we noticed spastic CP most common type of CP.
Cerebral palsy in children with normal birth weight was mainly caused by global ischemia secondary to perinatal asphyxia, cerebral malformation, intracranial bleed, and postnatal infections. This was comparable with other studies. ,
Cerebral palsy cases were equally observed from primary health centers and referral center (secondary/tertiary). Lack of timely intervention or referral at primary centers was observed. At referral center, more high risk cases had been delivered and very sick newborns had been managed resulting in neurological morbidity and CP.
All variants of spastic CP were observed in extremes of maternal age in our study. Pregnancy-induced hypertension (PIH) was observed in 6% of cases, which was comparable with previous studies  [Table 3]. Antenatal risk factors like PIH, infection, and drugs were predominantly known to cause vascular insult and thereby hypoxia resulting in spastic CP.
|Table 3: Comparison of incidence of risk factors and etiologies of cerebral palsy|
Click here to view
Birth asphyxia (hypoxic ischemic encephalopathy) was observed in 43% of cases and LBW in 30% cases which were comparable with a previous study  [Table 3]. Prematurity was observed in 15% of cases compared to 25.4% seen in Sharma et al., might be secondary to increased survival of morbid premature infants in their study.  Causes of prematurity could be extremes of age, maternal infections, familial, PIH, twinning, etc. Instrumentation was observed in 3% of cases compared to 7.5% in Sharma et al. study.  CP seen in 81% of vaginal deliveries might be due to lack of timely intervention in the perinatal period and nonavailability of appropriate obstetric and postnatal care.
Neonatal sepsis was observed in 4% of cases. Incidence of pyogenic meningitis and tubercular meningitis was 8% and 2%, respectively, which was comparable with Sharma et al. study.  Intracranial bleed during infancy was observed in 6% of cases and resulted in a unilateral form of CP (hemiplegia).
Classification of diagnosis
Eighty-one percent of the cases constituted a spastic variety of CP, which was comparable to Sharma et al.  and few international studies , [Table 4]. Bilateral spastic CP was the predominant type comparable to Sharma et al.  and few international observations. , Diplegia observed in 13% of cases compared to 54% in Sharma et al.  and 22% in few international studies , [Table 4]. Unilateral spastic CP constituted 9% in contrast with few international observations , [Table 4]. Hypotonia was observed in 12% of cases comparable with both Sharma et al.  and few international observations. , Dystonia in 5% of cases and mixed CP in 2% of cases, both were comparable with Sharma et al. and few international observations ,, [Table 4].
Intellectual sub-normality (IQ <70) was observed in 55% of cases. Other co-morbidities observed were, speech abnormalities in 38%, visual problems in 26% (strabismus, nystagmus, cataract, amblyopia, and cortical blindness), hearing impairment in 11% (sensorineural hearing loss), seizures in 46%, feeding problems in 19%, and undernutrition in 47% of cases. These were similar to Sharma et al.  [Table 5].
Intellectual subnormality and feeding problems were predominantly observed in bilateral spastic and hypotonic CP children [Table 5]. That was secondary to global cerebral involvement and cerebral malformations. Seizures were observed in 52% of bilateral spastic CP cases, 25% of spastic diplegic cases, 45% of unilateral spastic CP cases, and 50% of hypotonic CP cases, respectively. Lesser prevalence of seizures in spastic diplegia is probably because of the cortical sparing of the pathological events resulting in diplegia.  Our data is not representative of the community as it was done in a referral hospital. This is a limitation of our study.
| Conclusion|| |
Bilateral spastic CP was the most common clinical form of CP observed in our study mostly secondary to global ischemia during the perinatal period, which are mostly preventable. This is in contrast to the international observation of predominant unilateral spastic CP, which is mostly secondary to nonmodifiable intrauterine vascular insult.
Perinatal asphyxia is the important etiological factor in our study. We found preventable intranatal causes (60%) and antenatal causes (20%) formed a significant proportion of our study group. Hence, timely obstetrical intervention and immediate newborn care can still play a major role in preventing CP hence; there is an urgent need to further strengthen the existing maternal and child health services.
Co-morbidities are significantly observed in cases of CP. Appropriate screening and management of co-morbidities especially vision, hearing, speech, seizures, and nutrition improve the overall prognosis in cases of CP. Seizures add a dimension of uncertainty to the otherwise relatively static problem of CP.
Financial support and sponsorship
Conflict of interest
There are no conflict of interest.
| References|| |
World Health Organization. International Classification of Functioning, Disability and Health (ICF). Geneva: World Health Organization; 2001.
Surveillance of Cerebral Palsy in Europe. Surveillance of cerebral palsy in Europe: A collaboration of cerebral palsy surveys and registers. Surveillance of Cerebral Palsy in Europe (SCPE). Dev Med Child Neurol 2000;42:816-24.
NINDS Workshop on Classification and Definition of Disorders Causing Hypertonia in Childhood; 2001.
World Health Organization. International Classification of Impairment, Activity and Participation - ICIDH-2. Geneva: World Health Organization; 1980.
Rosenbaum P, Paneth N, Leviton A, Goldstein M, Bax M, Damiano D, et al.
A report: The definition and classification of cerebral palsy April 2006. Dev Med Child Neurol Suppl 2007;109:8-14.
Beckung E, Hagberg G. Neuroimpairments, activity limitations, and participation restrictions in children with cerebral palsy. Dev Med Child Neurol 2002;44:309-16.
Eliasson AC, Krumlinde-Sundholm L, Rösblad B, Beckung E, Arner M, Ohrvall AM, et al.
The Manual Ability Classification System (MACS) for children with cerebral palsy: Scale development and evidence of validity and reliability. Dev Med Child Neurol 2006;48:549-54.
Bartlett D, Purdie B. Testing of the spinal alignment and range of motion measure: A discriminative measure of posture and flexibility for children with cerebral palsy. Dev Med Child Neurol 2005;47:739-43.
Gorter JW, Rosenbaum PL, Hanna SE, Palisano RJ, Bartlett DJ, Russell DJ, et al.
Limb distribution, motor impairment, and functional classification of cerebral palsy. Dev Med Child Neurol 2004;46:461-7.
Ashwal S, Russman BS, Blasco PA, Miller G, Sandler A, Shevell M, et al.
Practice parameter: Diagnostic assessment of the child with cerebral palsy: Report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology 2004;62:851-63.
Hagberg B, Hagberg G, Olow I, von Wendt L. The changing panorama of cerebral palsy in Sweden. VII. Prevalence and origin in the birth year period 1987-90. Acta Paediatr 1996;85:954-60.
Hagberg B, Hagberg G, Olow I. The changing panorama of cerebral palsy in Sweden. VI. Prevalence and origin during the birth year period 1983-1986. Acta Paediatr 1993;82:387-93.
Sciberras C, Spencer N. Cerebral palsy in Malta 1981 to 1990. Dev Med Child Neurol 1999;41:508-11.
Riikonen R, Raumavirta S, Sinivuori E, Seppälä T. Changing pattern of cerebral palsy in the southwest region of Finland. Acta Paediatr Scand 1989;78:581-7.
Liu JM, Li S, Lin Q, Li Z. Prevalence of cerebral palsy in China. Int J Epidemiol 1999;28:949-54.
Ravn SH, Flachs EM, Uldall P. Cerebral palsy in eastern Denmark: Declining birth prevalence but increasing numbers of unilateral cerebral palsy in birth year period 1986-1998. Eur J Paediatr Neurol 2010;14:214-8.
Paneth N, Hong T, Korzeniewski S. The descriptive epidemiology of cerebral palsy. Clin Perinatol 2006;33:251-67.
Surveillance of Cerebral Palsy in Europe (SCPE). Prevalence and characteristics of children with cerebral palsy in Europe. Dev Med Child Neurol 2002;44:633-40.
Serdaroglu A, Cansu A, Ozkan S, Tezcan S. Prevalence of cerebral palsy in Turkish children between the ages of 2 and 16 years. Dev Med Child Neurol 2006;48:413-6.
Tuncbilek E, Ulusoy M. Consanguinity in Turkey in 1988. Nufusbil Derg 1989;11:35-46.
al-Rajeh S, Bademosi O, Awada A, Ismail H, al-Shammasi S, Dawodu A. Cerebral palsy in Saudi Arabia: A case-control study of risk factors. Dev Med Child Neurol 1991;33:1048-52.
Dowding VM, Barry C. Cerebral palsy: Changing patterns of birthweight and gestational age 1976-81. Br Med J 1988;297:25-9.
Pharoah PO, Cooke T, Rosenbloom L, Cooke RW. Effects of birth weight, gestational age, and maternal obstetric history on birth prevalence of cerebral palsy. Arch Dis Child 1987;62:1035-40.
Sharma P, Sharma U, Kabra A. Cerebral palsy - Clinical profile and predisposing factors. Indian Pediatr 1999;36:1038-42.
Hughes I, Newton R. Genetic aspects of cerebral palsy. Dev Med Child Neurol 1992;34:80-6.
Hagberg B, Hagberg G, Olow I, von Wendt L. The changing panorama of cerebral palsy in Sweden. V. The birth year period 1979-82. Acta Paediatr Scand 1989;78:283-90.
Edebol-Tysk K, Hagberg B, Hagberg G. Epidemiology of spastic tetraplegic cerebral palsy in Sweden. II. Prevalence, birth data and origin. Neuropediatrics 1989;20:46-52.
Himpens E, Van den Broeck C, Oostra A, Calders P, Vanhaesebrouck P. Prevalence, type, distribution, and severity of cerebral palsy in relation to gestational age: A meta-analytic review. Dev Med Child Neurol 2008;50:334-40.
Pharoah PO, Cooke T, Cooke RW, Rosenbloom L. Birthweight specific trends in cerebral palsy. Arch Dis Child 1990;65:602-6.
Paneth N, Rudelli R, Kazam E, Monte W. Brain Damage in the Preterm Infant. Cambridge: Cambridge University Press; 1994.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]