Neonatal brain damage, including the damage in the fetal period, is caused by many factors such as hypoxia, infection, trauma, intoxication and metabolic disorders. According to epidemiological studies, perinatal hypoxic-ischemic brain damage shows the highest incidence, and needs a new strategy for its prevention and treatment. This symposium is focused on the recent advances of basic research and technological science in the pathogenesis, neuroimagings, near-infrared spectroscopy, developmental neurophysiology, and intervention in perinatal hypoxic- ischemic brain damage, taking into consideration on the long term prognosis in each section.
It has been shown that nitric oxide (NO) generating cells are distributed widely in the brain and NO may act both as a neurodestructive and a neuroprotective agent in the pathogenesis of hypoxic-ischemic and reoxygenation injuries. Induction of hypoxia- ischemia dramatically increases NO production in brain. It is supposed that neuronally derived NO mediates glutamate neurotoxicity. The reaction of NO with superoxide can lead to neurotoxicity through formation of peroxynitrite which decomposes to form the cytotoxic oxygen free radical. On the other hand, NO mediates vasorelaxation and anti-thrombopoietic property and may protect against ischemic injury in this aspect. Some NO donors may also act as a protective agent through downregulation of NMDA receptor activity. These current studies suggest that some selective NO synthesis inhibitors or NO donors could be used in the novel treatment of hypoxic-ischemic brain injury.
Periventricular leukomalacia (PVL) is one of the neuropathological varieties of the neonatal hypoxicischemic encephalopathy. Recently we established a new canine model of PVL, by ligation of bilateral common, external and internal carotid arteries. In this paper we describe the relationship between neuropathological and neurological/behavioral findings of the PVL dogs.
Periventricular leukomalacia (PVL) has recently been recognized as an important risk factor of neurological impairment in premature infants. We studied 29 PVL cases on perinatal risk factors comparing with a non-PVL matched control group retrospectively. Variable decelerations were more frequently observed with statistical significance in the PVL group in the intrapartum period. Then another study was conducted to evaluate the relationship between fetal heart rate (FHR) decelerations and cystic PVL prospectively. Since January 1993 through December 1994 we studied 209 low birth weight infants (31.1±3.2 weeks, 1, 424±419g) who had been subjected to intrapartum FHR monitoring and postnatal sonographic intracranial examinations sequentially every 7 days until discharge. Cystic PVL was detected in 6 of 209 cases (2.9%) and occurred only in infants who had revealed severe variable deceleration or prolonged deceleration (6/37, 16%) in intrapartum FHR monitoring. We conclude that in low birth weight infants intrapartum severe variable deceleration or prolonged deceleration might play a causal role in cystic PVL.
Near-infrared spectroscopy, a new non-invasive technique, measures changes in the hemoglobin oxygenation state, blood volume, and redox state of cytochrome oxidase (cyt. ox.) in tissues. This technique now finds wide clinical applications, while the specificity and accuracy of the measurement of the redox state of cyt. ox. is still controversial. Recently, we have developed a new approach to measure the redox state of cyt. ox. This method has overcome several technological problems such as difficulty in determination of the in vivo absorption coefficient for cyt. ox. We describe here this new method briefly and the significance of the measurement of the redox state of cyt. ox. in the clinical medicine.