This is an umbrella term for permanent, nonprogressive but often evolving disorders of tone, movement or posture due to a cerebral insult to the developing brain – It is the most common chronic motor disability in childhood with prevalence of  2-3/1000 live births.  Causes of CP are given below.  No etiology can be found in 20-30% cases.

Genetic/ prenatal

• Genetic disorders
• Inborn errors of metabolism
• Structural malformations of nervous system
• Congenital/intrauterine infections
• Teratogens
• Maternal/obstetric complications

Perinatal

• Birth asphyxia
• Prematurity
• Low birth weight
• Birth trauma
• Neonatal infection
• Neonatal seizures
• Neonatal Hypoglycemia
• Intracranial hemorrhage
• Neonatal Hyperbilirubinemia

Postnatal

• Brain infections
• Hypoxia
• Trauma
• Drugs/ toxins/ metabolic disorders

Classification of CP:  There are various classification systems for CP.   Topographically there may be quadriplegia, hemiplegia, monoplegia, diplegia or triplegia.  Physiologically, CP may be spastic,  dyskinetic, ataxic or mixed. 

Clinical features:  The most common presenting complaint is developmental delay.  Persistence of neonatal reflexes and associated increased tone may be found.  Fisting of  hands with cortical thumb, scissoring of lower extremities, toe walking, abnormal postures and gait, abnormal movements and hyperreflexia may be present.  The clinical picture may be dominated by co-morbid conditions which include intellectual disability, microcephaly, seizures, behavioral problems, speech and language problems, sensory impairment such as blindness and deafness etc.  Apart from these, squints,  feeding and swallowing problems, malnutrition, sleep disorders and excessive drooling are often seen.   Contractures – initially dynamic and later fixed may form.

Spastic quadriplegia:  This is the most common type of CP in India. Etiology is often perinatal asphyxia or neonatal illness, and radiologically there may be cystic encephalomalacia. Severe intellectual disability, seizures, pseudobulbar palsy, microcephaly,  squint/visual disturbances, speech abnormalities and deformities are often found. 

Spastic diplegia is the next common type. This is often seen in premature babies and the radiological correlate is periventicular leucomalacia.  Intellect may be normal or near normal. 

Spastic hemiplegic CP is usually the end result of a vascular insult or perinatal stroke.  Weakness of one side of the body may go unnoticed till 12-24 months of age.  Early hand preference is a clue.  Neuroimaging usually reveals focal changes or a porencephalic cyst.  These children are usually ambulatory and intellect may be normal or impaired. 

Dyskinetic or extrapyramidal CP may result from asphyxia or neonatal kernicterus.  The patient has variable tone, posturing and prominent drooling.  Intellect may not be as much impaired  as it appears to be. Radiologically there may be atrophy or multicystic encephalomalacia or status marmoratus.

Ataxic CP:  Cerebellar signs are observed.  Etiology is often a cerebellar malformation.

Mixed CP: This refers to a mixture of spastic quadriplegia and extrapyramidal type of CP.

Evaluation:  A detailed history for manifestations and antecedent events, a full physical and neurologic examination and detailed developmental assessment is warranted in every child.  Dysmorphisms and neurocutaneous markers should be looked for.  Measurement of  Amiel Tyson angles by goniometer may reveal increased passive tone. Gross Motor Function Classification System (GMFCS) Modified Ashworth Scale (MAS) for spasticity and Manual Ability Classification Scale (MACS) are some scales for classifying severity.  The International Classification of Functioning, Disability and Health (ICF) can also be used to define the functional status of children with CP.  Neuroimaging should be done and is abnormal in upto 89% patients.  Common patterns observed are  cerebral atrophy,  multicystic encephalomalacia,  focal gliosis, periventricular leucomalacia and basal ganglia abnormalities.  Metabolic work up may be indicated when imaging is normal.  A thorough assessment of comorbidities should be done and documented.

Management:  A multidisciplinary team effort with holistic approach is required with involvement of occupational therapist, physiotherapist, clinical psychologist, orthopedic surgeon, orthotist, speech therapist, ophthalmologist, ENT specialist, social worker and special educator.  Generalised spasticity is managed by physiotherapy and drugs (diazepam, baclofen, tinazidine and dantrolene), while localized spasticity can be effectively treated with injection of botulinum A toxin into tight tendons every 4-6 months.  Dystonia is treated with trihexyphenidyl and levo-dopa. Surgical treatments in the form of tendon release and tendon lengthening operations are sometimes required.