Cerebral palsy defined as a non-progressive neuro-muscular disorder of cerebral origin. It includes a number of clinical disorders, mostly arising in childhood.
The essential features of all these disorders is a varying degree of upper motor neuron type of limb paralysis spasticity), together with difficulty in Coordination(ataxia) and purposeless movements.
Birth anoxia and injuries are the commonest cause of CP in developing countries. Causes can be divided into prenatal, natal and postnatal
Causes of cerebral palsy
|Prenatal causes||Defective development
|Natal causes||Birth anoxia
Pathology: The pathology of this disorder is the degeneration of the cerebral cortex or basal ganglion, either because of their faulty development or because of damage caused by the various factor.
Clinical features of Cerebral Palsy
Presenting complaints: The clinical features vary according to the severity of the lesion, the site of the neurological deficit and the associated defect
Severity of lesion: The lesion may be mild in 20 per cent of cases, in which case the child may remain ambulatory without any help and may never require consultation.
In the majority (almost 50 per cent of cases), the child requires help with ambulation.
The usual presentation is a child less than one year old, in whom the parents have noticed a lack of control on the affected limb.
There is a delay in the developmental milestones such as sitting up, standing or walking. In about 30 per cent of cases, the involvement is severe, and the child is bed-ridden.
Pattern of involvement: The pyramidal tracts are involved in 65 per cent of cases, and they present with spasticity, exaggerated reflexes etc.
One or all the limbs may be involved. The commonest pattern is a symmetrical spastic paresis of the lower limbs, resulting in a tendency to flex and adduct the hips (scissoring), to keep the knees flexed and the feet in equinus.
Less commonly, it may present as monoplegia, hemiplegia or quadriplegia. In the upper limb, there is typical flexion of the wrist and fingers with adduction of the thumb and pronation of the forearm.
In 35 per cent of cases, extra-pyramidal symptoms such as ataxia, athetoid movements, dystonia predominate.
Associated defects: These consist of speech defect, sensory defect, epilepsy, occular defects and mental retardation.
About 50 per cent of the patients are severely mentally retarded, 25 per cent have moderate mental retardation and 25 per cent have borderline mental retardation.
On examination, there may be weakness of muscles, the distribution of which is variable.
This leads to marked muscle imbalance, resulting in deformities. The joints are stiff because of spasticity; hence when a steady pressure is applied, the muscle relaxes and the deformity is partially corrected.
As the pressure is released, the spasm returns immediately. The tendon reflexes are exaggerated, and clonus may be present.
The patient exhibits a lack of voluntary control when asked to hold an object.
As the patient tries to move a single group of muscles, other groups contract at the same time (athetoid movements).
Mental deficiency may be present. There may also be defective vision and impaired hearing.
Principles of treatment: The aim of treatment is to maintain and develop whatever physical and mental capabilities the child has.
It consists of:
(i) orthopaedic treatment.
(ii) speech and occupational therapy.
Orthopaedic treatment consists of the prevention and correction of deformities, and keeping the spasticity under check. Methods of controlling the spasticity are:
(i) drugs-e.g., Diazepam, Beclofen
(ii) phenol nerve block
(iii) Neurectomy. Neurectomy may be required to control severe muscle spasm interfering with optimal rehabilitation.
Obturator neurectomy is performed for spasm of adductors of the thigh.
A number of other operative procedures may be necessary for improving selective functions.
Speech therapy and occupational therapy constitutes an important adjunct to the overall treatment of the child.
Mild cases can be looked after at home, but specialised residential schools are required for severely handicapped children.
Complete cure is impossible since an essential part of the brain is destroyed and cannot be repaired or replaced.
All that can be hoped for is improvement. Depending upon the severity of the underlying damage, a child can be made independent enough to earn his own living in due course.
A child formerly dependent on others for many daily activities may often become independent. This needs a great amount of patience and perseverance on the part of the parents and attendants of the child. In spite of all the treatment, there are a few in whom worthwhile improvement cannot be gained.