Cerebral palsy is a disorder that occurs in a period in child development, the motor cells in the central nervous system, is chronic and progressive is not due to abnormalities or defects in the brain tissue that has not finished growing. Although the cerebral lesions are static and not progressive, but the development of signs of peripheral neurons will change due to cerebral maturation.
Who first introduced this disease is William John Little (1843), who called it cerebral diplegia, as a result of prematurity or neonatal afiksia. Sir William Olser was who first introduced the term cerebral palsy, while Sigmund Freud called it Infantile Cerebral Paralysis.
Although difficult, the etiology of cerebral palsy need to know about preventive measures. Early physiotherapy give good results, but the mental developmental disorders can hinder the achievement of treatment goals.
Winthrop Phelps emphasized the importance of multi-disciplinary approach in the treatment of cerebral palsy sufferers, such as child discipline, nerve, eye, ear nose and throat, orthopedic surgery, neurosurgery, psychology, speech specialists, physiotherapists, social workers, school teachers Iuar usual. In addition it should also be included the role of parents and the community.
With the increase in obstetric care and perinatologi and low birth rates in developed countries such as Europe and the United States the incidence of cerebral palsy will decrease. But in developing countries, the progress of medical technology in addition to lowering the risk of infant mortality is high, also increased the number of children with developmental disorders.
The existence of variations in incidence in many countries because of cerebal palsy patients coming to clinics such as neurological clinics, children, orthopedic clinics, clinic medical rehabilitation and so on. Besides, because of clinicians do not consistently use the definitions and terminology of cerebral palsy.
There are several factors that influence the incidence of this disease are: the population is taken, how the diagnosis and thoroughness. For example the incidence of cerebral palsy in Europe (1950) as much as 2.5 per 1000 live births, while in Scandinavia as much as 1.2 to 1.5 per 1000 live births.
Gilroy have 5 of 1000 children showed motor deficits in accordance with cerebral palsy; 50% of cases, including light weight while 10% included. What is meant is that mild sufferers who can take care of himself, while the weight is classified as patients who require specialized care; 25% have average intelligence (normal), while 30% of cases showed an IQ below 70; 35% accompanied by seizures, while 50 % indicates the existence of speech disorders.
Men more than women (1,4:1,0). The incidence of relative cerebral palsy are characterized by complaints of motor is as follows: spastic 65%, atetosis 25%, and rigid, tremor, atactic I0% (9).
The cause of cerebral palsy can be divided into three periods, namely:
a) Congenital Malformations.
b) Infection in the womb which can cause fetal abnormalities (eg rubella, toksoplamosis, sifihis, cytomegalovirus, or other viral infections).
d) Tok gravidarum.
e) Asphyxia in utero (eg: solusio placenta, placenta previa, maternal anoksi, or abnormal umbilical cord).
b) intra-cranial bleeding.
c) the trauma of birth.
a) Trauma capitis.
b) Infections such as: bacterial meningitis, cerebral abscess, tromboplebitis, encephalomyelitis.
c) Kern icterus.
Several studies mention prenatal and perinatal factors contribute more than postnatal factors. Studies by Nelson et al (1986) (quoted from 13) mentions babies with low birth weight, asphyxia at birth, prenatal ischemia, genetic factors, congenital malformations, toxin, intrauterine infection is a causative factor of cerebral palsy.
Prenatal factors begins at gestation until birth, while the perinatal factors are all factors that cause cerebral palsy from birth to one month of life (11.13). Sedang1 post-natal factors ranging from the first month of life up to 2 years (Hagberg et al 1975), or up to 5 years of life (Blair and Stanley, 1982), or up to 16 years (Perlstein, Hod, 1964) (quoted from 12).
Clinical picture of cerebral palsy and depends on the extent of brain tissue damage
1) Paralysis. Hemiplegia can be shaped, kuadriplegia, diplegia, monoplegia, triplegia. This may be flaksid paralysis, spastic or mixed.
2) involuntary movements. Can be shaped atetosis, khoreoatetosis, tremor with tone that can be flaksid, rigidity, or a mixture.
3) Ataxia. Coordination disorder was caused by damage to the cerebellum. Patients usually show a decreased tone (hipotoni), and showed a delayed motor development. Started running very slow, and awkward all round movement.
4) Seizures. May be general or focal.
5) Impaired mental development. Mental retardation is found in approximately one third of children with cerebral palsy, especially in group tetraparesis, diparesis spastic and ataxia. Cerebral palsy is accompanied by mental retardation is generally caused by cerebral anoxia is long enough, resulting in an overall cerebral atrophy.
Mental retardation can still be repaired if damaged cerebral cortex is not complete and there are limbs that can be moved voluntarily. With the development of agile movements by a limb, mental development will be influenced positively.
6) may be obtained also vision problems (such as hemianopsia, strabismus, or refractive disorders), speech disorder, impaired sensibility.
7) emotional problems, especially during adolescence.
Many of the classification proposed by the experts, but on this occasion will be proposed classification based on clinical features and degree of functional ability. Based on the division of clinical symptoms of cerebral palsy are as follows:
1) Type of spastic or pyramidal. In this type of symptom that is almost always there are:
a) Hipertoni (folding knife phenomenon).
b) Hyper reflection accompanied klonus.
c) The trend arises contractures.
d) pathological reflex.
In topographic distribution of this type are as follows:
a) Hemiplegia if on the same side limb.
b) spastic diplegia. Regarding all four limbs, lower limbs heavier.
c) Kuadriplegi, on all four limbs, the limbs for a little more weight.
d) Monoplegi, when only one limb.
e) Triplegi when about one upper limb and two lower limbs, usually a variant and kuadriplegi.
2) Type of extrapyramidal
Will affect the shape of the body, involuntary movements, such as atetosis, dystonia, ataxia.
This type is often accompanied by emotional disturbance and mental retardation. In addition, also found hipertoni symptoms, hiperrefleksi mild, rarely to arise klonus.
In this type of contraction is rarely found, if the brain could be seen face asimetnis and disantni.
3) Type of mixture.
The symptoms are a mixture of both of the above symptoms, for example hyper reflection and hipertoni accompanied khorea movement.
Based on the degree of functional ability.
Patients can still perform daily pekerjaanlaktifitas It has none or very little need of special assistance.
Activity is very limited. The patient needs a variety of special assistance or special education in order
can take care of himself, can move or speak.
With the help specifically, the patient is expected to take care of yourself, walk or talk so it can move, hanging out, living in the community well.
Patients simply can not do physical activity and can not possibly live without the help of others.
Help or special education are given very little results. Such patients should be accommodated in special care homes. The house special is only for the treatment of patients with severe mental retardation, or which would cause social-emotional disturbance for both the family
and its environment.
Development of the nervous system begins with the formation of the dorsal neural tube of induction occurring at weeks 3-4 of gestation and the induction of ventral, took place at weeks 5-6 of gestation. Any disturbance in this period can result in congenital abnormalities such as kranioskisis totalis, anencephaly, hydrocephalus, and so forth.
The next phase of a proliferation of neurons, which occurs at 2-4 months gestation. Disturbances in this phase can lead to microcephaly, makrosefali.
The next stage is stage migration that occurred during gestational months 3-5. Migration occurs in two ways radially, sd differentiate and regional periventnikuler and subventrikuler into the inner layers of cerebral koerteks whereas tangential migration and differentiate sd germinal zone toward the surface of the cerebral cortex. Disturbances in this period can lead to congenital abnormalities such as polimikrogiri, agenesis of the corpus callosum.
Organizational stage of gestation occurred in the 6 months to several years postnatally. Disturbances in this stage will result in translocation of genetic, metabolic disorders.
Stage myelination occurs at birth until several years post-natal. At this stage occurs up to neurons proliferation, and formation mialin sheath.
Neuropatologik disorder that occurs depends on the weight and the severity of damage So neuropatologik abnormalities that occur are complex and diffuse to the motor cortex pyramidal tract area paraventnkuler basal ganglia, brain stem and cerebellum.
Cerebral anoxia often a intraventrikuler bleeding complications and perinatal asphyxia subependim often in combination with ischemia can cause necrosis.
Kerniktrus clinically give a yellow on the entire body and will occupy the basal ganglia, hippocampus, cells of the brain stem nuclei; can cause cerebral palsy type atetoid, hearing loss and mental retardation.
Infection can result in brain meningeal adhesions, resulting in obstruction of the subarachnoid space and arise hydrocephalus. Bleeding in the brain could be associated with left ventricular cavity.
Will lead to birth trauma or cerebral compression secondary tearing. Birth trauma is an irreversible cause symptoms. Another irreversible lesions due to trauma is happening sikatriks in cells of the cornu ammonis hippocampus, which could lead to resurrection of epilepsy.
Diagnosis is based on a complete history about a history of pregnancy, perinatal and postnatal care, and attention to risk factors for cerebral palsy. Also a complete physical examination with attention to motor and mental development and the presence of neonatal reflexes still persist.
In infants who have a high risk of examination is required repeatedly, because gejaladapat change, especially in infants with hipotoni, indicating that delayed motor development, almost all cerebral palsy through a phase hipotoni.
Another investigation that is needed is a plain head, lumbar puncture examination. Examination EEG, especially in pendenita showing motor symptoms, such as tetraparesis, hemiparesis, or because it is often accompanied by seizures. Ultrasound examination or CT head scans performed for head trying mencani etiology.
Psychological examination to determine the level of intellectual ability that will determine how education into regular schools or special schools.
There is no specific therapy against cerebral palsy. Treatment is symptomatic, which will hopefully improve the condition of the patient. Very early therapy can prevent or reduce neurological symptoms. To determine the type of therapy or training provided and to determine the success it is necessary to consider the classification of cerebral palsy based on the degree of functional ability that is mild, moderate and severe.
The goal of therapy is helping patients with cerebral palsy patients and their families to improve motor function and prevent deformity and emotional adjustment and education so pendenta few may require help from another, the patient is expected to be independent.
The drugs are given depends on the symptoms that arise. For example to be given anti-convulsive seizures.
For spasticity baclofen and diazepam can be given. When symptoms such as nigiditas can be given levodopa.
May be required surgical therapy for orthopedic and neurosurgical reconstruction of deformity that occurs.
Early and intensive physiotherapy to prevent disability, is also handling a psychologist or psychiatrist to cope with changes in behavior in older children. That should not be overlooked is the issue of education which should match the intelligence level of the patient. (kepri online daily)
By : I Made Oka Adnyana (kalbe.co.id)
Laboratory/UPF of Neurology Faculty of Medicine Udayana University/General Hospital Center Sanglah, Denpasar
Presented at a scientific meeting in order Anniversary VII Tumbuh Kembang Clinic, IKA Lab/FK Udayana University. Denpasar. dated 17 April 1993