Indian Pediatrics 1999;36: 1038-1042
Cerebral Palsy - Clinical Profile and Predisposing Factors
|Puneet Sharma, Usha Sharma, Ashok Kabra|
From the Department of
Pediatric Medicine, SMS Medical College, Jaipur, India.
Cerebral palsy is a static encephalopathy and may be defined as a non-progressive disorder of posture and movement, often associated with epilepsy and abnormalities of speech, vision and intellect resulting from a defect or lesion of the developing brain(1). The exact incidence and prevalence from our country is not known. This study was conducted to evaluate the clinical profile of cerebral palsy and to find out the various predisposing factors.
The present series was a retrospective study involving 480 cases of cerebral palsy. All the cases were thoroughly evaluated and the necessary investigations were done. Minear's classification of cerebral palsy(2), was used to classify and evaluate the patients. Associated handicaps such as subnormal intelligence, ocular defects, speech defects, deafness and convulsions were also noted.
The distribution of the cases of Cerebral Palsy is shown in Table I. Amongst the 480 cases studied, the sex ratio was observed to be 2.42:1. The athetoid, rigid, ataxic and mixed types of cerebral palsy were found only in males. One hundred and eighty two cases (38%) were first born. The head circumference was within 3 SD in 261 (54%) cases and was below 3 SD in 219 (46%) cases. Thirty two cases (6.7%) had high arched palate and other associated findings such as club foot, hydrocephalus, epicanthic folds etc. were found in 57 cases (11.9%).
Table I__ Distribution of Cases of Cerebral Palsy (n=480).
Subnormal intelligence was observed to be the most common handicap in our series (74.2%% of all the cases). Among the spastic cases, severe and profound mental retardation (IQ <35 and 20) was observed to be more common in quadriplegia (71.4% cases) and double hemiplegia (60% cases) as compared to diplegia (30% cases). All the patients of hypotonic, athetoid, rigid and mixed type of cerebral palsy were mentally retarded.
Convulsions were observed in 123 subjects (25.6%). The frequency of convulsions was 20.1% in the cases of spastic cerebral palsy, 50% in cases of mixed cerebral palsy, 62% in cases with hypotonic cereral palsy and 100% in cases of ataxic cerebral palsy. Other studies have reported highest incidence of convulsions in spastic type of cerebral palsy(3,4). Overall, the incidence of myoclonic seizures was observed to be the highest (9.2% of all the cases) followed by generalized tonic clonic seizures and focal seizures (6.9% of all the cases each).
A high prevalence of ocular defects has been reported in children with cerebral palsy. One hundred and seventy two cases (35.8%) had ocular defects with squint being the commonest (12% of the cases), followed by nystagmus and optic atrophy in 4.8% cases each and cataract in 6% of the cases. Eight per cent of the cases had other ocular defects such as refractive errors, chorio-retinitis, etc. All the 29 cases with cataract had history suggestive of intrauterine infection. Seven per cent of the children were blind without any obvious cause.
A high frequency of the speech defects was observed in our series (53.5% of all the cases). The highest frequency of speech disorders was observed in rigid type of cerebral palsy(100% of the cases) followed by hypotonic type (56%), spastic type (55.4%) and athetoid type (50%).
History of perinatal asphyxia was found in 48.7% of all the cases making it the single most common predisposing factor (Table II). Of these, 90% cases had spastic type, 7% cases had hypotonic type and 2.3% cases had athetoid type of cerebral palsy. Six per cent of all the cases were delivered by Breech delivery and history of Forceps applications, during delivery, was present in 7.5% of the cases, all of which were of spastic type. Infections emerged as the most common postnatal association of cerebral palsy (Table II).
Table II__Factors Predisposing to Cerebral Palsy
Figures in parantheses indicate percentages.
In the present study, among the spastic cases, mental retardation was found to be more severe in quadriplegia and double hemiplegia as compared to diplegia thus confirming the general rule that more the upper limbs are affected, lower is the intelligence(5).
A high frequency of speech defects was observed in our series. In cases of cerebral palsy, speech defects are multifactorial in origin, for example, impaired hearing, cortical damage, and incoordination or paresis of the muscles of tongue, lips, larynx and respiratory tract.
Various predisposing factors causing damage to the developing brain may lead to clinical picture of cerebral palsy and may act prenatally, natally or postnatally. The history of the other siblings suffering from cerebral palsy, present in some cases, may point towards the role of genetic factors, which are thought to contribute in about 2% of the cases(6). The well recognized familial forms of cerebral palsy are familial spastic paraplegia, familial athetosis and familial paroxysmal choreothetosis. In the present series, a family history of cerebral palsy was observed in 12 cases (2.5%) and all of them were of spastic type.
The majority of cases were observed to be due to factors acting during the birth process (Table II). Similar observations were made in other studies(7,8). The causal role of birth asphyxia in cerebral palsy has been questioned and asphyxia has been suggested to be a consequence rather than a cause of the process that leads to cerebral palsy(9). However, in the NCCP project, 20 minute Apgar of less than 3 was found to be associated with 250 fold increase in the risk of cerebral palsy(10). Case control studies comparing children with cerebral palsy with controls, for the markers of birth asphyxia, have suggested an asphyxial cause in 10% of the cases(11).
Low birth weight or gestation age have been associated with an increased risk of cerebral palsy(12). Several mechanisms could be responsible for a high incidence of cerebral palsy in children who were born premature. Premature neonates are more likely to suffer from birth asphyxia and injuries. A higher incidence of breech delivery, cord prolapse and precipitate labour in preterm delivery could expose the neonates to an additional risk of mechanical and asphyxial injuries. The underlying pathological lesions in these children are periventricular leukomalacia (PVL) and periventricular hemorrhagic venous infarcts (PHVI)(13).
In breech delivery, blood is squeezed from body towards the head so that the head enters the birth canal in extremely congested form. These congested vessels readily rupture. Also the umbilical cord is pressed when the head passes through the birth canal thus reducing the blood flow to the brain. Forceps application is known to cause cerebral contusion which may lead to cerebral anoxia.
In this series, infections emerged as the most common postnatal cause of Cerebral Palsy (Table II). Intracranial infections can either involve the blood vessels supplying different parts of brain thus leading to anoxic damage or can directly involve particular areas of brain. The importance of infections emerging as the leading postnatal cause of cerebral palsy lies in the fact that many of them are treatable.
In conclusion, this study revealed that the natal causes are the leading predisposing factors in cases of cerebral palsy. There is thus an urgent need to further strengthen the existing maternal and child health services in the country.
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