[Hypoxia during the perinatal period and the formation of cerebral lesions].

The degree of hypoxia and the cerebral blood flow are of outstanding importance in the pathogenesis of cerebral damage due to perinatal hypoxia. Nevertheless many other factors influence origin, extension and localisation of cerebral damage. An acute total ischemia results especially in disorders of brainstem, inferior colliculi and thalamic nuclei while the most frequent type, the partial ischemia, manifests in cortical regions. In immature newborn infants, posthypoxic lesions are usually located periventricular, in mature infants, cortically. Brain edema preferentially occurring in mature infants damages CNS additionally. This danger is enhanced by supplementation of glucose before hypoxia resulting in accumulation of even more lactic acid. Intracerebral hemorrhages predominantly occur in immature infants. One speculates that they are caused by rupture of thin capillary walls of germinal matrix. Due to impaired autoregulation of cerebral blood flow after perinatal hypoxia, these vessels are exposed to every change of arterial blood pressure. Therefore therapy of metabolic acidosis and posthypoxic circulatory insufficiency may contribute to intracerebral hemorrhage too.