Causes of Cerebral Palsy: Origins, Etiology, Aetiology, Causal Pathways
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
Cerebral Palsy
“Postneonatally acquired cerebral palsy accounts for a significant proportion of all cerebral palsy. It is no less severe and is equally disabling as congenitally acquired cerebral palsy, with a similar mortality rate to 5 years….In less developed societies, postneonatally acquired cerebral palsy is principally due to cerebral infection and febrile convulsions in infancy. As societies develop, causes change and diversify rather than disappear entirely. Infectious causes become less important, and head injury becomes more important. Small numbers also result from causes that might previously have been fatal. The strong association with social disadvantage make it likely that postneonatally acquired cerebral palsy is primarily a social disease of poverty and ignorance combining to create barriers to effective parenting.”

-Stanley, Blair & Alberman

Cerebral Palsy

Cerebral Palsy
The paths to cerebral palsy not needing to be associated with fetal effects or birth trauma include CNS infection, haemophilus influenzae meningitis, H. influenzae type b, Streptococcus pneumoniae, Neisseria meningitides, pertussis, immunization against pertussis, Reye snydrome, ALTE, and QT syndrome. Other factors include asphyxia, hypoxia, exposure to toxic chemicals, head injury, cerebral hemorrhage, malnutrition, seizures, convulsions and dehydration following gastroenteritis, near drowning, accidental suffocation, electrocution, and shock following a burn.

“Postnatal factors known to be associated with both preterm birth and cerebral palsy but which are unlikely to be markers of prior causes or early measures of the outcome include patent ductus arteriosus, hypotension, blood transfusion, prolonged mechanical ventilation, pneumothorax, sepsis, shock, hyponatraemia, total parenteral nutrition, hypoglycaemia and low blood serum thyroxine…..While some of these may merely be indicators of severity of morbidity (as has been suggested for hypothyroxinaemia) rather than causes of cerebral palsy in themselves, others are plausibly factors which interfere with cerebral blood flow (Leviton and Paneth 1990) or result in brain damage from infection or inflammation. Thus these postnatal complications may well be causal pathways to white matter damage, the majority of which is initiated postnatally.” (Stanley, Blair & Alberman, p.81)

Even cerebral palsy believed to be derived from events occurring after the neonatal period can have womb origins. Postneonatally acquired CP children show lower than normal birth weight, respiratory problems or CNS abnormalities. Some of these children may have been made vulnerable to those CP inducing traumas by earlier influences. It is also possible that an occasional vulnerable child is a result of modern medicine’s ability to bring to health children born very prematurely.

“Data from hospitals and clinics suggest that cerebral infections and febrile convulsions are the most common causes in African countries. Duggan and Ogala (1982), citing four African studies, mentioned only meningitis and febrile convulsions, though not all cases were accounted for. Makwabe and Mgone (1984) in Tanzania, and Dyer (1997) in Zambia highlighted cerebral malaria as the principle cause of febrile convulsions. Sathiakumar and Yakuba )1987), on the other hand, reported that five of their northern Nigerian series of seven postneonatally acquired cases had had septicaemia. In India, Laisram et al. (1992) reported a similar pattern with 74 per cent due to cerebral infection and 16 per cent due to convulsions (cause not specified), but the remaining 10 per cent were attributed to head injury. In Turkey, Ozmen et al (1993) reported that more than half of 300 postneonatally acquired cases had had either meningitis or septicaemia…..” (Stanley, Blair & Alberman, p.130)

In countries where the populations are a mix of races exposed to widely divergent care, studies reveal how postneonatal cerebral palsy is acquired differently by different social stratus. 1.6 times more Atlanta Blacks than Whites acquired cerebral palsy postneonatally. In South Africa 2.6 times more Blacks than Whites reflected this same result. The rate of Aboriginal acquisition of CP in later childhood from factors unrelated to birth or natal issues was 8 times the White population.

Infection and head injury are two of the most common sources at this age. Head injury usually occurs after the age of 2, infection before 2. Half of the cases before age 5 occur in the first year. One study reported that 27 percent of the postneonatal cases happen between ages 5 and 10. H. influenzae type b, Streptococcus pneumoniae, Neisseria meningitides and Strep pneumoniae are all common sources of these infections. Particularly vulnerable to these CNS infections are children with nutritional & immune system problems, and children needing hydrocephalus operations. Trauma can also come in the form of a physical blow to the head or shaken baby syndrome.

“Severe infections, especially meningitis or encephalitis, can also lead to brain damage in this age group. Meningitis is inflammation of the meninges (the covering of the brain and the spinal cord), usually caused by a bacterial infection. Encephalitis is brain inflammation that my be caused by bacterial or viral infections. Either of these infections can cause disabilities ranging from hearing loss to CP and severe retardation.” (Miller & Bachrach, p.11)

Asphyxia can also influence this group when food becomes lodged in the throat, a near drowning occurs, or poisoning.


Stanton, Marion, (2002) The Cerebral Palsy Handbook. Vermillion

Stanley, Fiona, Blair, Eve, Alberman, Eva. (2000) Cerebral Palsies: Epidemiology & Causal Pathways. Mac Keith Press

Blair, E., Stanley, F. (1982) ‘An Epidemiological study of cerebral palsy in Western Australia, 1956-1975. III: Postnatal aetiology.’ Developmental Medicine and Child Neurology, 24, 575-585

Arens, L.J., Molteno, C. D. (1989) ‘A comparative study of postnatally-acquired cerebral palsy in Cape Town.’ Developmental Medicine and Child Neurology, 31, 246-254.

Pharoah et al. (1989) ‘Acquired cerebral palsy’ Archives of Disease in Childhood. 64, 1013-1016

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Causes of Cerebral Palsy: Origins, Etiology, Aetiology, Causal Pathways