Jaisle F
Z Geburtshilfe Neonatol. 1996 Sep-Oct;200(5):169-75.
The "perinatal asphyxia" is regarded to be one of the causes of cerebral palsy, though in the very most of the children with cerebral palsy there is found no hypoxia during labour. It should be mentioned, that the definition of "perinatal" and "asphyxia" neither are unic nor concret. And also there is no correlation between nonreassuring fetal heart rate patterns and acidosis in fetal blood with the incidence of cerebral palsy. Numerous studies in pregnant animals failed in proving an acute intrapartal hypoxia to be the origin of the cerebral palsy. Myers (1975) describes four patterns of anatomic brain damage after different injuries. Only his so called oligo-acidotic hypoxia, which is protracted and lasts over a longer time is leading to brain injury, which can be regarded in analogy to the injury of children with cerebral palsy. Summarising the update publications about the causes of cerebral palsy and the studies in pregnant animals there is no evidence that hypoxia during labour may be the cause of cerebral palsy. There is a great probability of a pre(and post-)natal origin of brain injury (for instance a periventricular leucomalacia found after birth) which leads to cerebral palsy. Short after labour signs of a so called "asphyxia" may occur in addition to this preexisting injury and misrepresent the cause of cerebral palsy. Finally the prepartal injury may cause both: Cerebral palsy and hypoxia.
“围产期窒息”被认为是脑瘫的病因之一,尽管在绝大多数脑瘫患儿中,分娩期间并未发现缺氧情况。应该指出的是,“围产期”和“窒息”的定义既不统一也不具体。而且胎儿心率异常与胎儿血液酸中毒和脑瘫发病率之间也没有相关性。对怀孕动物进行的大量研究未能证明急性分娩期缺氧是脑瘫的起因。迈尔斯(1975年)描述了不同损伤后大脑解剖损伤的四种模式。只有他所谓的低酸性缺氧,即持续时间较长的缺氧,会导致脑损伤,这种损伤可类比脑瘫患儿的损伤。总结关于脑瘫病因的最新出版物以及对怀孕动物的研究,没有证据表明分娩期间的缺氧可能是脑瘫的病因。脑损伤很有可能起源于产前(和产后)(例如出生后发现的脑室周围白质软化),进而导致脑瘫。分娩后不久,除了这种先前存在的损伤外,可能会出现所谓“窒息”的迹象,从而误判脑瘫的病因。最后,产前损伤可能导致两种情况:脑瘫和缺氧。