Cerebral palsy has been defined as “persistent and non-progressive disorder of posture and movement due to an insult sustained by the developing brain”. Developmental and genetic factors are responsible in large percentage of cases (90%) while only 10% of cases are due to intra partum damage.

It is a developmental disorder present at birth or in early childhood in which lesions (Degeneration / imperfect development of nerve cells) of the various parts of the brain (cerebral cortex, basal ganglia, cerebellum) cause developmental defects of motor functions.

These disturbances may range from mental retardation varying in severity, generalized spastic rigidity, spastic diplegia affecting the legs, hemiplegia to various forms of extra pyramidal dysfunction (chorea, athetosis tremors, ataxia) depending on the site of lesion.

1. Risk factors: Prenatal, perinatal or postnatal.

2. Motor milestones are delayed (normal milestones: Head up at three months (2) sifting unaided at six months (3) crawling by eight months (4) walking 12-15 months).

3. Three varieties:

(a) Spastië diplegia (Little’s disease)

(b) Spastic hemiplegia

(c) Congenital athetosis, ataxia and chorea 4. Persistence of primitive reflexes


The disease is often apparent at the time of birth. There are various factors which account for the disease. These are:

1. Premature or precipitate birth leading to Hypoxia.

2. Trauma due to prolonged birth from uterine inertia.

3. Eclampsia during pregnancy

4. Birth injuries leading to hemorrhage or anoxia of the brain

5. Rubellain early months of pregnancy

In only 5-10% of the cases, cerebral palsy develops after birth and here the main conditions are encephalitis, Kemicterus, prolonged convulsions or coma.

Clinical features

As a rule, features of the disease are not recognized until some months after birth. The disease is noticed when the child fails to reach the normal milestones of development. Thus there is failure to hold the head up at 3 or 4 months and to sit up at 6 to 7 months. These are often the first signs.

As the child grows the signs of disease become apparent and there is noticed stiffness of the limbs, rigidity and peculiar movements of the limbs. Child’s failure to walk, talk and mental deficiency draws attention to the condition. The disease may present clinically in various forms.

1. Spastic diplegia (Little’s disease)

There is involvement of pyramidal tracts with increased spasticity of the lower limbs. The child has a tendency to walk on toes with knees mbbing together and the legs are often crossed (scissor gait). The tendon reflexes are exaggerated and clonus is present. Contractures also develop in the spastic muscles. Mental deficiency is an important feature.

2. Spastic Hemiplegia

It is an uncommon condition. Involvement is generally of one limb where involvement of upper limb takes place earlier as compared to lower limb. Parents notice this condtion when the child makes attempt to walk. Mental retardation is there but less as compared to cerebral diplegia. Other conditions in this group include spastic monoplegia (only one limb affected) or spastic quadriplegia where are four limbs are affected.

3. Congenital bilateral Athetosis, Ataxia and Chorea

These signs are suggestive of basal ganglia and cerebellar involvement. These lesions are recognized only after several months or a year has elapsed. Child presents with irregularity of movements and involuntary movements (Athetosis, chorea) or features of cerebellar ataxia (flaccid limbs Intention tremors). Very often all these features may be present in mixed form. Such children have predominant features of intention tremors, general awkwardness and difficulty in controlling the voluntary movements.

Besides the above form of clinical syndromes of cerebral palsy (cerebral diplegia, choreo-athetosis, cerebral ataxia), child has features of mental deficiency. Convulsions of various types are frequently seen. These children are usually late in acquiring control of the sphincters.


It is not difficult since cerebral palsy is present since birth or during the first months of life and has characteristic clinical picture (increased spasticity of limbs, scissor gait, mental retardation, Delayed milestones). Differentiation may be mode from Polio, amyotonia congenita and progressive spinal muscular atrophy.


Although the neurological damage by and large is non-progressive but the disability is not. The brain does recover from early insults but this has its limitations and once brain damage has occurred it cannot be reversed.

The main problem is due to spasticity of muscles and the effects it has on the development of bones and joints. The thrust of treating cerebral palsy is at treating the effects of neurological lesions rather than the lesion itself. Main aim is to lessen the disability. Those who show progressive degeneration, there is no treatment available.

In the presence of rigidity, treatment be directed towards prevention of contractures by stretching and correct positioning of joints. Child must be taught gradually simple procedures such as holding of hand, grasping, balancing the head and sitting and standing. Child be gradually trained in walking so that he does not injure himself.

Toilet habits have also to be looked into. Medical treatment consists of administration of Botulinum toxin to be injected into muscles under general anaesthesia or under sedation. The most commonly injected muscle groups are the hamstrings, the calf muscles and the hip adductors.

The effect lasts for three to six months and injection then can be repeated. Botulinum acts by irreversibly binding to the receptor at the neuromuscular junction causing relaxation of the spastic muscles.

Other drug being used is baclofen (a gamma amino butyric acid agonist) which works by restoring the balance of excitatory and inhibitory input to reduce muscle hyperactivity. It is useful as a muscle relaxant especially in cases with spastic quadriplegia. It is given intrathecally by an intrathecal catheter linked to a reservoir of baclofen implanted into the abdomen. In this method infection is a serious complication.

Where there are much contractures and deformities, tenotomy lengthening of tendons, neurotomy and arthrodesis are beneficial.

Physiotherapy in the form of massage and voluntary movements (Both active and passive) should be employed. Rigid apparatus for prevention of deformity and to reduce contractures is not advisable. Tenotomy should always be followed by massage and passive movements. It should not be performed till a fair degree of voluntary power is present.

For convulsions anti-epileptic drugs are employed. When choreo athetoid movements are very distressing, chlorpromazine in small doses be given.

Prognosis. It shall depend on the degree of disability the child suffers from. Chances of improvement are good especially in mild cases. Earlier the treatment is instituted better the prognosis.