Cerebral palsy (CP) is a neurodevelopmental disorder that begins in early childhood and lasts throughout life. Its history can be traced back to ancient Egypt, as depicted in drawings from the 5th century BC.1 Dr. John William Little (1810-1894), an orthopedic surgeon inspired by his own disability, wrote the initial medical reports on CP in 1861. It was originally called 'Little's disease’.2

The international Executive Committee for the Definition of CP describes “a group of permanent disorders of the development of movement and posture causing activity limitations that are attributed to non-progressive disturbances that occurred in the developing fetal or infant brain. The motor disorders of cerebral palsy are often accompanied by disturbances of sensation, cognition, communication, perception, and/or behavior, and/or by a seizure disorder”.3

Globally, CP is the most common cause childhood disability affecting children in the low-and-middle income countries (LMIC) .4,5 The estimated global prevalence is between 1.64 and 3 per 1000 live births, with higher rates documented in Africa, as shown by a population-based study in Uganda.4, 5, 6 The incidence of CP is 70 times higher among premature neonates with a birth weight of less than 1500 grams compared to those with a birth weight above 2500 grams.7 In LMIC, neonatal mortality rates are high, and the mortality rates for preterm infants are even higher.8 Thus, in contrast to high-income countries where survival rates are higher, premature neonates in LMIC often die. Consequently, premature neonates contribute less to the total number of children with CP in LMIC.

Birth asphyxia leading to hypoxic ischemic encephalopathy (HIE) is still the primary risk factor for CP in LMIC, followed by neonatal jaundice. Other risk factors leading to CP that have been reported include prematurity, congenital brain malformations, genetic and metabolic abnormalities.9, 10, 11, 12 Birth asphyxia leading to HIE has been reported to cause multiorgan dysfunction including cardiac, renal, hepatic and hematological which may persist in later childhood.13

CP is classified physiologically into spastic, dyskinetic and ataxic based on the area of the brain that is predominantly affected (Fig. 1). Spastic, Dyskinetic and Ataxic CP affects predominantly the cortex, basal ganglia and cerebellum respectively.7,14,15 The most common physiological type is the spastic CP accounting for 70-80 % of cases, followed by dyskinetic at 15-20 %, ataxic at 5 %, and mixed (spastic and dyskinetic) at 10-15 %.9,16,17 Additionally, CP is classified based on the anatomical distribution of the motor impairment, whether it is unilateral (previously called hemiplegic) or bilateral and based on the number of limb involvement into monoplegic, diplegic, triplegic and quadriplegic subtypes.3,7 The most common subtype is the quadriplegic subtype accounting for 50-60 % followed by hemiplegic 20-30 % and diplegic at 5-10 %.16

The severity of CP is assessed using various functional classification systems. These include the Gross Motor Function Classification System (GMFCS), which evaluates gross motor function; the Manual Ability Classification System (MACS), which assesses upper limb function; the Communication Function Classification System (CFCS), which evaluates everyday communication abilities; and the Eating and Drinking Ability Classification System (EDACS), which assesses the ability to eat.14,15,18,19 Determining the severity is important in evaluating the level of function of the affected child and the outcome of treatment. Determining the level of function is important in predicting prognosis and services required for rehabilitation.18 The classification is graded from level I, where the affected child is fully independent, to level V where the child is fully dependent.18

The static lesions in children with CP cannot be reversed; therefore, managing children with CP focuses on addressing motor impairments, sensory deficits, and associated comorbidities. The objective of the management is to improve functional ability, enhance independency and prevent or minimize complications. Early identification and early intervention are crucial in management of children with CP as it addresses the disease process at its earliest stage and facilitates the neuroplasticity of the brain.20,21

Management of CP in LMIC is limited by the poverty levels, inadequate paediatric neurology services, stigma and the social-cultural beliefs about its aetiology. Despite these challenges, locally developed and adaptable cost-effective interventions can greatly enhance the quality of life for children with CP and their families.22,23