The causes of cerebral palsy and diffuse preterm brain injury are unknown. In very preterm infants, brain insults that result from haemorrhage and or local ischemia may predispose to the development of cerebral palsy in over 50% of cases, identifiable by two years of age. Obstetric mishap is usually blamed. However, the European Cerebral Palsy study (Bax, Tydeman and Flodmark, 2006) identified the lesions as prenatal or less than 40 weeks, hence the bulk cannot be due to obstetric mishap and are far more likely a consequence of adverse nutritional or infectious conditions. The very preterm infant is also known to suffer long-term effects from disordered brain development, some of which may be diffuse, possible impairment of neurogenesis and connectivity, or due to white matter lesions (Dammann et al., 2010; Aarnoudse-Moens et al., 2009; Maalouf et al., 1999).
A popular hypothesis is that cerebral palsy results from a systemic, inflammatory response to infection, viral or bacterial, remote from the brain (Cowan, Leviton and Dammann, 2000; Nelson et al., 1998; Duggan et al., 2001). Although causes of brain damage in very preterm infants may be pre- or postnatal, considerable research has failed to produce direct evidence of a role for prenatal infection, suggesting other factors may be more important. None the less, malnutrition and infection are frequent partners, the one exacerbating the other.
Cerebral palsy occurs more frequently in multiple gestations, jeopardising fetal nutrition. The co-existence of other congenital anomalies has led to the suggestion of fetofetal transfusion problems in a monochorionic multiple gestation and the concept of a vanishing twin (Pharoah, 2005; Pharoah, 2007). Biochemical studies on preterm infants similarly have provided evidence of vascular compromise in the very preterm infant, due to: (i) maternal insufficiency prenatally, and (ii) the failure of post-natal infant nutritional management to replicate the essential lipids required for vascular growth and integrity (Crawford et al., 2003).
The commonest complications of prematurity start with vascular disorders or at least involve vascular/immune dysfunction, viz. intraventricular haemorrhage, periventricular leukomalacia, retinopathy of prematurity (obliteration of the retinal blood vessels), bronchopulmonary dysplasia (leaking fibrin from pulmonary vessels) and necrotising enterocolitis (immune and vascular systems in inflammation).
Despite the advances in medicine and science, there has been no progress in prevention or treatment of cerebral palsy, the incidence of which has barely changed since the late 1980s, having then escalated several fold since 1967 (Pharoah et al., 1990).The same applies to allied neurodevelopmental disorders, with mental ill health now a major burden of ill health.
For references see Bibliography.