The term 'periiventricular leukomalacia' (PVL) usually covers necrotic
and/or gliotic lesions from perinatal origin occurring in the periven
tricular ring of telencephalic white matter. PVLs are found post-morte
m in one third of brains from autopsies of premature infants; PVLs are
diagnosed in 4 to 10% of infants born before 33 weeks of gestation an
d remaining alive more than 3 days after birth. PVL is very rare in at
term infants. The proportion of PVLs from prenatal origin is estimate
d between one third and one half of cases. Recent progresses in neuroe
pidemiology, developmental neurobiology and imaging methods permit to
revisit the pathophysiology of PVLs on a multifactorial basis. The fin
al result of these multiple factors seem to be calcium influx due to g
lutamatergic overactivation triggered by cytokines, infection and infl
ammation, and deficit in neurotrophic factors. Periventricular topogra
phy can be explained by properties of intracerebral vascular wail at t
his stage of angiogenesis and by perfusion failure/hypoxia. (C) 1998,
Elsevier, Paris.