The paths to cerebral palsy not associated with fetal effects or birth trauma include central nervous system infection, hemophilus influenzae meningitis, H. influenza type b, Streptococcus pneumoniae, Neisseria meningitidis, pertussis, immunization against pertussis, Reye’s syndrome, apparent life-threatening event (ALTE), and Long QT syndrome (a condition affecting the electrical system of the heart).  Other factors include asphyxia (insufficient oxygen to the brain), hypoxia (reduction in blood supply), 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 pre-term birth and cerebral palsy but which are unlikely to be markers of prior causes or early measures of the outcome include patent ductus arteriosus [a congenital heart defect], hypotension [low blood pressure], blood transfusion, prolonged mechanical ventilation, pneumothorax [collapsed lung], sepsis, shock, hyponatremia [a reduction in the sodium level of the plasma], total parenteral nutrition [intravenous feeding], hypoglycemia [lower than normal level of glucose in the blood], 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.  (Alberman, Blair, and Stanley)

Even cerebral palsy believed to be derived from events occurring after the neonatal period can have womb origins.  Children with postneonatally acquired cerebral palsy show lower than normal birth weight, respiratory problems, or central nervous system abnormalities.  Some of these children may have been made vulnerable to cerebral palsy-inducing traumas by earlier influences.  It is also possible that a child is more vulnerable as a result of modern medicine’s ability to sustain children born very prematurely.

Data from hospitals and clinics suggest that cerebral infections and febrile convulsions (convulsions caused by fever) 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 principal 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 septicemia (infection of the bloodstream).  In India, Laisram et al. (1992) reported a similar pattern with 74 percent due to cerebral infection and 16 percent due to convulsions (cause not specified), but the remaining 10 percent 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 septicemia.  (Alberman, Blair, and Stanley)

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 groups.  In Atlanta, 1.6 times more blacks than whites acquired cerebral palsy postneonatally.  In South Africa, 2.6 times more blacks than whites acquired the condition postneonatally.  The rate of Aboriginal acquisition of cerebral palsy in later childhood from factors unrelated to birth or natal issues was 8 times the acquisition by the white population.

Infection and head injury are two of the most common sources.  Head injury usually occurs after the age of two, infection before two.  Half of the cases before age five occur in the first year.  One study reported that 27 percent of the postneonatal cases happen between ages five and ten.  H. influenza type b, Streptococcus pneumoniae, and Neisseria meningitidis are all common sources of these infections.  Particularly vulnerable to these central nervous system infections are children with nutritional and 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 may be caused by bacterial or viral infections.  Either of these infections can cause disabilities ranging from hearing loss to CP and severe retardation."  (Bachrach and Miller)

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.

Cooke, T.; Pharoah, P.; and Rosenbloom, L.  “Acquired Cerebral Palsy.”  Archives of Disease in Childhood 64 (1989):1013-16.

Hart, Hilary M., ed.  Clinics in Developmental Medicine.  London:  Mac Keith Press.   Alberman, Eva; Blair, Eve; and Stanley, Fiona.  Cerebral Palsies: Epidemiology and Causal Pathways.  London:  Cambridge University Press, 2000.  (The book is part of a series of hardcover monographs published by Mac Keith Press.  Four new ones are published each year.  The distributor is Cambridge University Press.)

Stanton, Marion.  The Cerebral Palsy Handbook:  A Practical Guide for Parents and Carers.  London:  Vermillion, 2002.