Cerebral palsy is a disorder of motor control resulting in abnormalities in posture, muscle tone, and motor coordination. It results from an injury or an abnormality occurring to the motor regions of the immature brain. The definition assumes that the causal "injury" is prenatal, perinatal, or neonatal, but some clinicians have extended the time of injury up to the first several years of life. It is also a general requirement that the insult to the central nervous system leading to cerebral palsy be a nonprogressive insult, and that the injury be circumscribed in time. However, as is frequently the case, both the time of the "injury" and the nature of the "injury" may be elusive, or as we often state under such circumstances, the cause is "idiopathic."
Cerebral palsy is a clinical syndrome and not a distinct disease entity. Its hallmark is motor impairment resulting from a significant injury to the pyramidal and/or extrapyramidal systems. Known causes are vascular, traumatic, and toxic/metabolic events, while other possible causes may be teratogenic. The diagnosis of cerebral palsy generally presumes that genetic disorders have been ruled out.
Children with cerebral palsy frequently have other associated handicaps. When the brain injury is more extensive, there may be visual, hearing, and cognitive impairments. Many children have speech and language difficulties as well. In addition, electrophysiologic disturbance may lead to epilepsy. While clinically difficult to diagnose, some children with cerebral palsy also have parietal sensory deficits.
Cerebral palsy is most frequently classified according to the predominant neurologic sign. Abnormalities in muscle tone and extrapyramidal functions lead to a descriptive classification. Table 1 lists the various types of cerebral palsy. The classification of spastic cerebral palsy is further refined by considering the number of limbs involved. Quadriplegia refers to four limb involvement, hemiplegia to involvement of the arm and leg on one side, diplegia to predominant leg involvement, and monoplegia to single limb involvement. In one study of cerebral palsy 53% of children had spastic diplegia, 28% spastic quadriplegia, and 10% spastic hemiplegia.1 All other types combined, accounted for only 9% of cases.
CLASSIFICATION OF CEREBRAL PALSY
When the pediatrician is confronted with a child with delayed or abnormal motor development it is important to distinguish between central and peripheral causes, and between nonprogressive and progressive entities.2
Cerebral palsy is a "central" disorder implying that the primary defect is in the motor areas of the brain involving the pyramidal or extrapyramidal systems. "Peripheral" implies that the cause of the motor abnormality is located in the peripheral nervous system. This includes the anterior horn cell, peripheral nerve, neuromuscular junction, and muscle.
ABNORMAL MOTOR DEVELOPMENT
Central versus Peripheral
To diagnose cerebral palsy, which is a primary example of a central lesion, there are certain neurologic signs that need to be identified. Increased deep tendon reflexes are generally present. In a peripheral neuropathy or a myopathy, deep tendon reflexes tend to be absent or decreased. In addition, contractures of joints tend to manifest more frequently with central disorders than peripheral disorders. Muscle atrophy tends to be more prominent with myopathies or neuropathies. Delays in adaptive and social functions as well as in language generally suggest a central disorder. The presence of fasciculations, especially of the tongue, would tend to suggest a peripheral or anterior horn cell disorder. Increased muscle tone is seen classically with central disorders. Decreased muscle tone is more frequently seen with peripheral neuropathies and myopathies but on occasion it can be seen in "benign central hypotonia" which is a poorly delineated disorder. The hypotonia is found in association with delayed development as well as frequent cognitive difficulties. In hypotonic cerebral palsy, the situation would be similar. In such conditions, however, one can once again rely on deep tendon reflexes, for they would tend to be increased in the central forms of hypotonia.
Table 2 summarizes these parameters for differentiating central versus peripheral nervous system disorders. It is also important to note that mental retardation itself can result in delayed motor development. Frequently, there will be a relatively uniform delay not only in motor functions but also adaptive, language, and social functions.
Certain historical factors can also help to refine the difference between central and peripheral processes. Problems with feeding in infancy tend to be noted with central nervous system lesions and cerebral palsy. The infants may be irritable and tend not to be "cuddly."
Nonprogressive versus Progressive
Cerebral palsy is one of many chronic, non-progressive (static) encephalopathies. If there is prematurity or suggested evidence of trauma at delivery or anoxia, a cerebral palsy can be hypothesized. However, we can cite the case of an infant who had profound hypotonia and swallowing difficulties in infancy, who had a history of a traumatic delivery. As the child developed, the hypotonia persisted and there were delayed motor milestones. It was only when obesity became apparent between 2 and 3 years of age that the diagnosis of Prader-Willi syndrome was made. Therefore, while the history is one of the most critical parameters for diagnosis, it can also be misleading. It is most important to note that with non-progressive cerebral conditions, while motor development is delayed, it is unusual to ñnd regression. In certain progressive neurologic disorders, regression may not occur until later childhood, and in fact, may be masked early on by maturation of various brain centers. Questions regarding familial consanguinity and similar problems in the family are important since such questioning may lead to the diagnosis of a genetic degenerative disorder. Pes cavus, neurocutaneous stigmata, and scoliosis in the family may be clues to such entities.
EARLY SIGNS OF CEREBRAL PALSY
We will not elaborate in great detail on the early signs of cerebral palsy since another section in this journal deals with this matter in depth. However, a brief summary is in order. It is important to note that the primary defect in cerebral palsy is a lack of inhibition oí teleologically less sophisticated motor areas of the central nervous system. These centers reside in the lower parts of the brain and spinal cord. In fact, many of the signs of cerebral palsy are most likely due to a release of spinal cord centers from cerebral control. Primitive reflexes and postural reactions reflect the normal functioning of these areas. With normal maturation, we expect these responses to be modified by time as upper motor neuron systems exert their influence. However, when there has been an injury, to these upper motor neuron systems and inappropriate control results there is a persistence of primitive reflexes such as the asymmetric tonic neck response, Moro response, palmar grasp, and lack of evolution of more sophisticated responses. As a consequence, various postural and protective reflexes do not evolve in a normal fashion. Asymmetry also reflects abnormality and the lack of upper motor neuron control on one side. Exaggerated primitive reflexes also imply that the spinal cord regions are uninhibited.
TYPES OF CEREBRAL PALSY
In discussing the various types of cerebral palsy, it is important to note that while we depend on various neurologic signs to classify the type of cerebral palsy, there may be changing signs that confound the diagnosis. For example, it has been noted that children who develop hypertonic cerebral palsy will on occasion be hypotonic initially.3 This has been referred to by some authors as the "latency period. " The clinician finds that the child is hypotonic until approximately 6 to 9 months of age at which time hypertonia begins to manifest itself. If this potential change in tone is not appreciated then one may misconstrue that there is a degenerative disorder present. Children with athetoid cerebral palsy may also have variable tone in early infancy and not manifest the movement disorder until a later date. For example, children with kemicterus may be hypotonic or hypertonic during infancy and it is only between 2 and 3 years of age that athetoid movements manifest. This is noted in other basal ganglia or extrapyramidal disorders as well, where there is a general tendency for the involuntary movements not to reveal themselves until later in childhood. The cause for this is not clear. While this evolution is present in certain cases of cerebral palsy, it is also of significance that degenerative diseases may follow the same pattern. For example, children with Lesch-Nyhan disease are most frequently hypotonic early in infancy and then begin to develop rigidity and subsequently choreoathetosis. In contradistinction to the above patterns of evolution in tone and movement, if a child is found to have hypertonia and then subsequently develops hypotonia, this should alert the clinician to the possibility that a degenerative disease is present. It would be unusual to find such a change in tone in children with static encephalopathies. An example of such an abnormal evolution is found in children with metachromatic leukodystrophy and other leukodystrophies. There is a primary degenerative disorder of the brain and upper motor neuron system leading to hypertonia and hyperreflexia. Since metachromatic leukodystrophy may also be associated with a peripheral neuropathy that clinically presents at a later date, there is a progressive hypotonia from the nerve disorder as well as a gradual decrease in deep tendon reflexes.
RISK FACTORS OF CEREBRAL PALSY
DIFFERENTIAL DIAGNOSIS OF CEREBRAL PALSY
Children with spastic quadriplegia are frequently microcephalic. They are at great risk of mental retardation, seizures, and pseudobulbar palsy. In pseudobulbar palsy there is paresis of facial, lingual, and pharyngeal muscles making feeding and speech very difficult. Recurring pneumonias may intervene because of difficulty in the handling of secretions. The child is at great risk of not being able to sit or walk. Ocular problems are relatively frequent with optic atrophy, nystagmus, and strabismus. Children with extensive cerebral injury may also have cortical blindness from damage to the visual centers of the occipital lobes.
Spastic hemiplegia is very difficult to diagnose in the first 3 months of life. Even if there is hemiparesis, movements of the extremities may be normal because of mediation through lower brain centers. Asymmetry of deep tendon reflexes and persistent fisting may be the earliest signs. Brachial plexus injury may be mistaken for hémiplégie cerebral palsy but a flaccid arm with decreased deep tendon reflexes is suggestive of a peripheral nerve injury. Difficulties occasionally arise when the traumatic delivery responsible for the brachial plexus injury also results in cranial trauma and possible brain injury. Between 6 and 9 months of age, persistent fisting and asymmetry of lateral propping and parachute responses will tend to confirm hémiplégie cerebral palsy. There is often a persistent palmar grasp response on the affected side. The heel cord and other leg muscles will be hypertonic compared to the normal side. Handedness before I year of age is always suspect although, interestingly, we have seen infants and toddlers with left-handedness where there is a similar family history. Hemiplegia may be so mild as to escape detection until walking is achieved. The affected leg drags and there may be toe-walking. In addition, there may be "paretic posturing" of the affected arm with flexion at the elbow and a decrease in the natural arm swing. Almost all children with hémiplégie cerebral palsy learn to walk. Children are at risk of developing focal seizures, visual field defects, cortical sensory deficits, and scoliosis. Many of the children also have learning disabilities with perceptual impairment. If hémiplégie cerebral palsy is acquired subsequent to the perinatal period (ie, meningitis, trauma, etc.), there is a much greater potential for development of epilepsy than in the congenital type.
Since the legs are primarily involved in spastic diplegia, gait is more affected than hand skills. It is almost always the result of complications prior to or during delivery. Prematurity and small gestational size for age also contribute significantly. Acquired forms are rare. In early infancy, scissoring with tightness of the adductors of the thighs and general spasticity of the legs is noted. There is frequently bilateral ankle clonus. Ambulation is greatly influenced by intellectual capabilities. Orthopedic intervention is almost always necessary to achieve ambulation.
Ataxic Cerebral Palsy
This is a relatively rare form of cerebral palsy. Frequently there is hypotonia initially. Cognitive problems are generally present. Of primary importance is to rule out hydrocephalus or a rare congenital tumor. Macrocephaly would be especially suggestive of the above entities. The earliest signs of cerebral dysfunction are truncal ataxia and titubation of the head where there is a fine bobbing noted. When head bobbing is prominent, certain lesions of the third ventricle need to be considered, especially a colloid cyst which is amenable to surgery. As the children develop, tremor with reaching may become prominent. Ataxia developing in a progressive fashion is almost always suggestive of a degenerative or progressive neurologic condition.
Choreoathetoid Cerebral Palsy
With the advent of prevention of kernicterus, pure choreoathetoid cerebral palsy has decreased in frequency. Anoxia, however, can result in choreoathetoid cerebral palsy and in mixed type cerebral palsy with choreoathetosis and spasticity. Quite often the children are hypotonic in infancy and as mentioned, athetosis develops later. Interestingly, we have seen one child with hyperglycinemia and another with a rare metabolic disorder, sarcosinemia, presenting with choreoathetosis prior to I year of age. Children destined to have choreoathetoid cerebral palsy often have a persistence especially of the asymmetric tonic neck response or an obligate response. In addition, there is frequently paresis of upward gaze. In severe cases of choreoathetoid cerebral palsy, there is opisthotonos with arching of the back. In addition, there are abnormal dyskinetic movements of the facial muscles, tongue, and palate leading to grimacing, swallowing, feeding, and speech difficulties. Complicating phonation even further is a lack of coordination of the respiratory muscles and an erratic breathing pattern. The picture of facial grimacing, drooling, and lurching movements frequently leads to an erroneous diagnosis of associated mental retardation. This is compounded further by the speech problems. However, as is the case in all children with cerebral palsy, careful psychological assessment is indicated for many of the children have normal or near normal intelligence and can communicate and learn effectively with special aids.
Various perinatal risk factors have been identified as being associated with cerebral palsy. Table 3 lists these risk factors. While a careful history will often delineate the etiologic basis for cerebral palsy, frequently no risk factors can be identified. Illustrative of this, is that in hémiplégie cerebral palsy the cause may be unknown in up to 30% of children.4
While cerebral palsy can be identified at a relatively early age, it is important to monitor the progress of diagnosed children. Certainly, the non-progressive nature of the neurologic condition has to be documented over time. In the differential diagnosis of cerebral palsy it is important to consider not only progressive degenerative diseases but also various chronic non-progressive encephalopathies that may also mimic cerebral palsy. Table 4 is a partial list for the differential diagnosis of cerebral palsy.
In spastic quadriplegia, non-progressive disorders that need to be considered are various dysmorphic syndromes, congenital infections, disorders of dysgenesis of the brain (ie, agenesis of the corpus callosum, porencephaly), and metabolic disorders (ie, hypoglycemia, leukodystrophies, Menkes Kinky Hair Syndrome). In children with spastic hemiplegia, incontinentia pigmenti, porencephaly, and SturgeWeber Disease need to be ruled out.
In patients with predominant choreoathetosis, one needs to consider Lesch-Nyhan Disease and Wilson's Disease. Various forms of hypoparathyroidism and hypocalcémie syndromes can also lead to choreoathetosis and unusual movement disorders. In children with hypotonic-atonic type of cerebral palsy the clinician needs to consider the possibility of an underlying amino or organic aciduria, mucopolysaccharidosis, anterior horn-cell disease, and myopathic disorder.
In children with the ataxic type of cerebral palsy, hydrocephalus, Arnold-Chiari malformation, tumors, and other degenerative disorders need to be sought. With dystonic types of cerebral palsy, HallervordenSpatz Disease, Wilson's Disease, and dystonia musculorum deformans need to be considered. While the potential differential diagnosis for cerebral palsy as can be seen is relatively extensive, its clinical manifestations are specific enough that in general it is easily diagnosed.
Children with spastic quadriplegia frequently have cystic degeneration of central white matter. There is often cortical involvement as well.5 Some patients have porencephalic cysts communicating with the ventricles. It appears that anoxic injury is frequently involved as are abnormalities in regional blood flow. Deep periventricular injury occurs most frequently in immature infants, while cortical injury predominates in term infants. 6 Children with spastic diplegia tend to have periventricular injury of the internal capsule. Premature infants are most susceptible. Patients with spastic hemiplegia tend to have atrophy of the opposite cerebral hemisphere and a vascular injury is generally hypothesized.
In those patients with anoxic encephalopathy leading to choreoathetosis, basal ganglia injury predominates. The caudate nuclei and putamen show degeneration. When there is also spasticity, deep white matter and cortical injury may be observed. When kernicterus is the etiologic basis of choreoathetosis, there is pigmentary degeneration of the basal ganglia, dentate nuclei, and other brain stem nuclei.
It is very difficult to delineate the work-up that is indicated when one is confronted with a child with a suspected cerebral palsy. A strong history of risk factors, a lack of a similar family history, and the presence of a typical clinical picture and examination may be sufficient to make the diagnosis of cerebral palsy. On the other hand, many families will request a work-up and a possible explanation. Given the chronic nature of the disorder and the potential prognosis, an initial, comprehensive investigation may be warranted in a significant number of children.
Rather than cite an arbitrary list of recommended tests, it would appear to be more appropriate to list various neurologic tests and to indicate in what way they may be helpful in the work-up of cerebral palsy.
Computerized axial tomography of the brain may provide greater enlightenment as to the basis of cerebral palsy. There may be porencephaly, a gross malformation, an old infarction, or hydrocephalus. On rare occasions, especially in children with macrocephaly, an unexpected congenital brain tumor may be identified. In addition, in children with café-au-lait spots, and macrocephaly, aqueductal stenosis with dilatation of the ventricular system may be identified in association with neurofibromatosis. Intracranial calcifications can lead to the diagnosis of congenital in utero infections such as cytomegalovirus or toxoplasmosis. Children with such infections generally have microcephaly. Subependymal calcifications are found in tuberous sclerosis. As part of the work- up, a Wood's lamp examination would appear to be appropriate in those children with abnormal development, associated seizures, and mental retardation. When depigmented spots are identified, Wood's lamp examination of the parents is also important given the genetic implications of tuberous sclerosis.
If laboratory tests are contemplated there should be a primary focus on "treatable causes." Serum copper and ceruloplasmin determinations should be obtained in children with unexplained choreoathetosis. Thyroid function studies are especially appropriate in children with hypotonia. A serum uric acid is indicated in those youngsters who have hypotonia and subsequent athetosis. Serum qualitative amino acid analysis and a metabolic investigation of the urine are suggested in children with hypotonia especially in the setting of delayed social and cognitive maturation and somnolence that is unexplained. When recurrent vomiting and/or somnolence occur a serum ammonia, pyruvate and lactate may delineate a hyperammonemia syndrome.
Serologic tests may further identify the presence of a congenital infection. The skull x-ray in general is not helpful but on occasion various syndromes with abnormal calcium metabolism and mucopolysaccharidoses may be identified in this manner. The use of the electroencephalogram in this setting is interesting. One would tend to think that it is not indicated, but when one is confronted with a child with hypotonia where there is confusion as to whether there is a peripheral or a central basis for the abnormality in tone, an abnormal electroencephalogram may point to cerebral causes. Certain patterns on the electroencephalogram may also suggest a degenerative disorder. A careful ophthalmologic examination may reveal chorioretinitis suggestive of cytomegalovirus, rubella, or toxoplasmosis infections. Degenerative diseases may also be identified in the context of a retinopathy. A cherry-red spot in the macular area may be suggestive of Tay-Sachs Disease or metachromatic leukodystrophy. In children with spastic hemiplegia a visual field defect can be identified in this manner.
Audiologic investigation is indicated especially in children with kernicterus and hyperbilirubinemia, cytomegalovirus infections, and rubella. Chromosomal analysis should be obtained in children with dysmorphism to delineate various genetic disorders. It is becoming increasingly apparent, however, that on occasion children with relatively few dysmorphic features may also have chromosomopathies that are associated with delayed and abnormal motor development. As an example, Fragile-X syndrome, which is being increasingly identified in various developmental conditions may present with very few dysmorphic features. While classically there is coarse facies with macrogenitalia we have seen a number of children where the clinical diagnosis has been quite difficult because of more subtle findings.
Cardiologic assessment may reveal an associated cardiac defect especially in congenital infections and certain chromosomopathies. All children should have psychological testing to delineate any intellectual or learning problems.
It is interesting to note that prognosis is often determined not by the extent or nature of the motor deficit but rather by the presence of associated symptoms. For example, when there is significant mental retardation, even though the motor deficit can potentially be overcome, a nonambulatory state may result. Seizures may also take their toll, especially when they are of the mixed type. Certain children develop mixed-type seizures with akinetic drop attacks and various minor motor seizures leading to Lennox-Gastaut syndrome on the electroencephalogram. This syndrome is frequently associated with neurologic regression even though a true degenerative disease cannot be delineated. Visual handicaps with optic atrophy, nystagmus, and field defects may also significantly affect motor development and learning. Abnormalities in hearing will have significant effects on the evolution of social and cognitive capabilities. Secondary orthopedic complications with evolving contractures can result in motor deterioration even though there is no progressive encephalopathy. As a consequence, one may see a child with spastic diplegia who is able to stand and take steps but is later nonambulatory because of contractures.
The clinician will find that parents will frequently ask for prognosis at an early age. Most physicians will understandably be uncomfortable in such a situation. Prognostication is one of the most difficult areas in the management of cerebral palsy. Each clinician adds to his lexicon of knowledge regarding cerebral palsy with each new patient that one encounters. It is important to be able to follow many patients through childhood and adolescence to be able to develop one's own understanding of the broad spectrum of potential outcomes. Unfortunately, while the "experience" of the seasoned clinician helps in the development of a coherent approach to prognostication, such experience over time is also a humbling experience for one sees more and more cases where eventual outcome is unpredictable. One child may appear to have severe problems in infancy with difficulty in feeding, muscle tone, and delays in all areas of development only to find several years later that the parents return with a social, interactive, and ambulatory child. One may note that certain parents exude confidence, are stubborn in the face of "overwhelming odds," and have a "naive faith" in the ability of caring and human persistence to triumph over insurmountable handicaps. When the eventual outcome is better than the physician expected it is appropriate to wonder whether such parental persistence can overcome certain odds, or whether it was merely the clinical impression that was invalid. We have all seen families where the parents appear to be the "deciding factor" in outcome. In other families, we may just as easily wonder whether pessimism may not become a self-fulfilling prophecy.
In contradistinction to the above examples, we have also experienced frequent cases where initial hopes for a given child were optimistic yet where projected goals were never achieved. In many such cases, there was a lack of appreciation of the extent of associated intellectual impairment.
In the past several years various studies have been reported which may ultimately provide more objective parameters to assist the physician in prognostication. In one study of infants less than 1 , 500 g, CT scans were performed after certain criteria were met.7 Forty-three percent were found to have cerebral intraventricular hemorrhage (CVH), 17% of these infants died by 1 year of age, 6% of infants without hemorrhage also died. It was found that infants with Grade 1 CVH (germinal matrix hemorrhage), and Grade 2 CVH (intraventricular hemorrhage with normal ventricular size) did not have an increased risk of "major handicaps" at follow-up. In infants with Grade 3 CVH (intraventricular hemorrhage with ventricular dilatation) and Grade 4 CVH (intraventricular hemorrhage with parenchymal hemorrhage) there was a direct relationship to major handicaps at between 12 to 24 months of age. Major handicaps were not only related to cerebral palsy but also seizures, severe visual or auditory deficits, and significant mental impairment.
In another study of infants under 1,500 g admitted to a neonatal intensive care unit,8 the significance of periventricular low density (PVLD) was studied. PVLD has been related to periventricular leukomalacia seen in the setting of asphyxia. Infants were followed to 18 months. Infants in Group I (normal CT scan) in general had normal scores at 18 months on Bayley Scales of Infant Development. Infants with focal frontal and occipital PVLDs had similar scores. Infants with similar diffuse low density white-matter lesions tended to have as a group developmental abnormalities. How this relates to cerebral palsy, however, is not well-delineated by the authors.
In a third study of 435 infants born at =£34 weeks gestation, cystic leukomalacia was associated with severe cerebral palsy and mental retardation in all affected infants.9 Such cysts could be diagnosed by 3 to 6 weeks of age with cranial ultrasound. Cystic degeneration of periventricular areas is generally a sign of anoxic injury. An interesting part of this study was that 9/18 infants surviving severe periventricular and intraventricular hemorrhage were normal, 7/18 had mild-to-moderate handicaps and only 2/18 had severe handicaps. This study shows that severe cystic PVLD associated with ischemia tends to cause severe handicaps, while the prognostic implications of intraventricular hemorrhage are much more difficult to ascertain.
It is obvious from the above discussion that the physician should share with families the significant uncertainties in prognosis. Various areas of the brain where myelinization and dendritic proliferation have not yet taken place during infancy and early childhood cannot be clinically tested. The degree of remaining "plasticity, " or capacity for uninjured areas of the brain to assume certain functions of injured areas cannot be predicted. The need forclose follow-up by the pediatrician and appropriate specialists has to be emphasized. It is important to stress that such close follow-up and linear observation will ultimately help delineate the prognosis. It will also identify on a timely basis any special needs that must be addressed, and are necessary for the prevention of secondary complications in orthopedic, psychological, and learning areas.
While uncertainty manifests in a significant number of cases, there are many children who demonstrate certain abnormal neurologic signs and developmental patterns from which a gloomy outcome is apparent from the initial examination.
In considering overall prognosis, long-term followup of large populations with cerebral palsy, does show a generally discouraging outcome if one considers achievement of competitive employment in adulthood.10,11 With the advent of computers, however, and more effective methods of assisted communication, motorized wheelchairs, and special aids, it would appear that the next several decades will yield significant advances in this area. There is true potential for the development of various competitive and productive vocational opportunities.
1. Franco S. Andrews BF: Reducción of cerebral palsy with neonatal intensive care. Clinical Research 1975; 24:66A.
2. Taft LT. Barabas O: Infants with delayed motor performance. Pediatr CUn North Am 1982; 29:137.
3. Molnar GE, Taft LT: Pediatric rehabilitation part 1: Cerebral palsy and spinal cord injuries. Curr Pro« Pediatr 1977; 7(3).
4. Hagberg B. Hagberg G. Olow 1: The changing panorama of cerebral palsy in Sweden 1954-1970. II. Analysis of the various syndromes. Acta Poediotr Scand 1975; 64:193.
5. Benda CE: Developmental Disorders of Mentation and Cerebral PaUy. New York, Grune and Stratton. 1952.
6. Towbin A: Central nervous system damage in the human letus and newborn infanr: Mechanical and hypoxic in]ury incurred in rhe fetal-neonatal period. Am / Dis Child 1970; 119:529.
7. Papile L, Munsick-Brvno G, Schaefer A: Relationship of cerebral intraventficular hemorrhage and early childhood neurologic handicaps. J Pediatr 1983; 103:273.
8. McCarton-Daum C, Danziger A. Ruff H. et al: Periventricular low density as a predictot of neurobehavioral outcome in very low-birrhweight infants. Dev Med Child Neurol 1983; 25:559.
9. Knshamoorthy KS. Shannon DC, DeLong GR, et al: Neurologic sequelae in the survivors of neonatal intraventricular hemorrhage. Pediatrics 1979; 64:233.
10. Ingram TS: ftdiomc Aspects of Cerebral Palsy. Edinburgh, Livingston. 1964.
11. O'Reilly DE: The adult with cerebral palsy.Dev Med Child Neurol 1974; 16:707.
CLASSIFICATION OF CEREBRAL PALSY
ABNORMAL MOTOR DEVELOPMENT
RISK FACTORS OF CEREBRAL PALSY
DIFFERENTIAL DIAGNOSIS OF CEREBRAL PALSY