Cerebral Palsy is a generic term that is applied to a non-progressive motor disorder. Approximately (2).% of children born today will have some form of cerebral palsy (CP). There are four main categories in which CP disorders are placed. First, Spastic syndromes due to upper motor neuron involvement are representative of 70% of CP cases (8). Subgroups of this include hemiplegia (21%), quadriplegia (27%), and diplegia (21%), which is a mixture of quadriplegia and paraplegia (8). The hemiplegics of this group often have mild or less severe speech impediments than the other subgroups (8). Second, athetoid and dyskinetic syndromes occur in about 20% of the cases (8). This group has the slow, writhing movements and choreiform like movements of the distal extremities also (8). These movements cease during sleep and increase when they become upset. Speech impairment is also often found in these patients (8). Third, ataxics’ (10%) have cerebellar involvement, wide based gait, intention tremors, problems doing fine movements, and incoordination weakness (8). Fourth, mixed forms of the above named groups are the most common, with spastic and athetoid symptoms being the most often paired. Convulsive seizures are often found in CP patients which often adds to the problems (8). Other associated problems include cognitive impairment, vision and hearing impairments, problems with communication, emotional deficits, behavioral problems and feeding problems (3). Spastic hemiplegics and paraplegics are the most likely to be of normal intelligence (3). Hemiplegics have the lowest incidence of mental retardation with about 40% of them (3). In CP patients it appears that the higher the degree of spasticity the greater the other problems will be (3). Sixty-six percent of the CP patients are mentally retarded (3). Of these patients, 50% are severely retarded, 35% are moderately retarded and the remaining 15% are mildly retarded (3). Most of the remaining CP patients with "normal intelligence" have perceptual problems and must be placed in learning disability classes (3).
Several theories have been given as to the cause of CP. These include; neonatal jaundice, genetics, infections of infancy, neonatal asphyxia, and birth trauma. Neonatal jaundice causes bilirubin encephalopathy (kirnicterus) which is not common today with Rh immunization and other clinical advances that prevent the massive lysis of child RBC’s (3). Genetic causes of CP have been linked to an autosomal recessive gene in a few cases of the ataxic diplegia form (4). Infancy attributions include head trauma and meningitis (3).
The original thought was that CP was a result of birth trauma and the physician’s competence was a large factor in the incidence of CP. It appears that only 6% of CP cases are due from intrapartum events but most of these seemed to originate their etiology from prenatal or postnatal factors (5). This conclusion comes from the fact that CP children had similar Apgar scores except for acidosis of the veins in approximately 18% of the CP children compared to 0 in normal children (5). This may be due to a lack of equipment to actually diagnose the acidosis, especially in cerebral acidosis. Also, C-sections do not protect against CP and are not advised unless they are normally applicable (5). Another study found that many babies are subject to a sudden lack of oxygen at birth and most of these children are fine (2). This points to possible correlation’s between predisposing factors that may have made the child more susceptible to the lack of oxygen than the lack of oxygen itself, or had nothing to do with the intrapartum lack of oxygen. Together, these form a lack of association between birth events and CP. If any correlation’s can be made, many more studies must be performed to come up with this correlation since "inappropriate" intrapartum care occurs equally in the birth of CP children as it does in the birth of normal children (5).
The latest data suggest that the most prevalent cause of CP are in utero effects. There are a few documented cases of spastic cerebral palsy in pregnancy such as rubella infections, iodine deficiency and maternal methyl mercury exposure (1). Other predisposing factors are premature birth, and low birth weight, and poor maternal nutrition and care. These may combine to interfere with fetal growth and therefore its brain development, or the fetuses with damaged or defective motor areas of the brain may cause the poor growth in utero. Powell et. al. discovered the risk of spastic diplegia increases with both lowered gestational age and lowered birth weight, but lowered gestational age increases the risk more than lowered birth weight has for CP (6). This may be a result of increased number of births towards term than birth weight being a factor, because both lowered and normal birth weight peaked in CP incidence in close to term time (6). Another study showed that CP rates reach levels as high as 4% in infants with a weight less than 2500 grams (6). But this may be due to lowered birth weight of premature infants combined. The cause of the premature infants may be due to a "Diplegia Factor" or lack of, may cause premature labor and/or cause impaired growth and development in utero (6). The other possible highly likely cause is poor mother nutrition. One study pointed to the fact that the mother’s nutrition level at or right before conception correlates more with the result of CP (2). Fetal cord blood of low birth weight infants with small head circumference had deficient levels of arachidonic acid (2). The study also found that low levels of arachidonyl phosphoglycerol correlated with low birth weight, low levels of docosahexaenyl glyceride correlated with premature birth, and that endothelial ethanolamine phosphoglycerides related to fetal growth of "historical interest" in the future (2). Those are a few of the deficient fats to be considered, but the amounts and number of fats needed for proper growth in utero are very substantial. One very interesting point is that pre-formed fatty acids (one’s recently ingested) are incorporated ten times faster than the parentally formed fatty acids (2). Essential fatty acids such as linoleic and linolenic are very important in the growth of brain tissue and blood vasculature (2). Pre-term infants are often denied adequate levels of arachidonic acid, docosahexaenyl glyceride, linoleic and linolenic acid because they have no constant placental supply so the membrane integrity is compromised and growth is compromised (2). These correlate well with the high proportion of cerebral hemorrhages that occur in premature infants (2). These may also be a cause of CP in these premature infants. Crawford studied 500 pregnancies and found that the mothers producing low birth weight babies were deficient in 43 of 44 different vitamins, minerals, and fatty acids when compared to mothers producing normal birth weight babies. Another strong correlation was that the mothers that smoked produced low birth weight babies partly because there nutrient intake was lower (2).
One thing of interest that has been learned because of CP is that perinatal hemiplegia damage to either the right or left side didn’t exhibit the normal deficiencies exhibited by similarly located lesions in the adults (7). The extent of the cerebral damage perinatally had a lesser amount of correlated defects than was found with the presence of seizures or very abnormal EEG readings, which appeared to be the most important correlation to the severity of the neurological damages (7). These though, may have been due to the seizures. or the fact that these children were on seizure medications (7). In fact, the defects were few and mild even with the large lesions in children with no seizures or very abnormal EEG readings (7). These findings show the great amount of plasticity that the brain have to teach the non-injured side things that are normally on the other side, but it also shows its limitations, in that crowding occurs on the unaffected side decreasing the patients ability to perform the functions normally associated with that position on the opposite lesioned half of the brain (7). Example: The left (dominant) brain is damaged in Broca’s area so the speech center shifts to the corresponding right side which is associated with visual-perceptual and spatial functions. The patient would have deficiencies in one or both of these functions to some degree because of crowding.
Early detection is very important to CP patients so rehabilitating measures can be initiated. The warning signs are premature birth, low birth weight, excessive lethargy, irritability, high pitched cry, decreased interest in the surroundings, poor head control, asymmetric movements, unusual posturing, a weak suck, tongue thrust and a tonic bite (3). Later, the gross and fine movements are abnormal and delayed for age, or they use one hand almost exclusively (3). Most cases of CP are diagnosed by one year of age (3). Current treatment for CP patients include medications for seizures, spasticity, constipation, and gastroesophageal reflux related to the spasticity associated with the CP patient (3). These patients often require other extensive medical help (3) including; orthopedic and neurosurgery consultations and treatments (3), speech therapy, and occupational therapy to help the CP patients with the oral-motor, visual-perceptual and daily living problems (3). Physical therapy is used for treatment to control associated posture and tone problems.
The causes and correlation’s of CP are being more known to us so that we now have a good idea to some of the major causes and problems associated with CP, but a lot of research still needs to be done in this area if we are truly ever going to completely understand the causes of Cerebral Palsy. "It is time to stop looking for our keys under lamp-posts, because the causes of the majority of cerebral palsy cases do not currently lie in well illuminated places (1). We must look at new places and find new ways of testing our old knowledge if we are ever to completely understand Cerebral Palsy.
BIBLIOGRAPHY:
1. Blair, E. and Stanley, F. Intrauterine growth and spastic cerebral palsy II. The association with morphology at birth. Early Human Development. 1992, 28: 91-103.
2. Crawford, M. Essential Fatty Acids and Neurodevelopmental disorder. Adv. Exp. Med. Biol., 1992, 318: 307-14.
3. Eicher, P. and Batshaw, M. Cerebral Palsy. Pediatr. Clin. North- Am., 1993, Jun; 40(3): 537-548.
4. Hughes, I. and Newton, R. Genetic Aspects of Cerebral Palsy. Dev. Med. Child Neurol., 1992, Jan; 34(1): 80-86.
5. Melone, P., Ernest, J., O’Shea, M., Klinepeter, K. Appropriateness of intrapartum fetal heart rate management and risk of Cerebral Palsy. Am. J. Obs. Gyn., 1991 (Aug.), 165: 272-277.
6. Powell, T. et. al. Cerebral Palsy in Low-birth weight Infants. II. Spastic Diplegia Associations with Fetal Immaturity. Developmental Medicine and Child Neurology, 1988, 30:19-25.
7. Vargha-Khadem, F. et. al. Development of intelligence and Memory in Children with Hemiplegic Cerebral Palsy. Brain, 1992, 115: 315-329.
8. The Merck Manual, Pediatrics and Genetics, Chpt. 198, pg. 2110.