HI發(fā)生發(fā)展及影像診斷

1、概述窒息缺氧心輸出量減少hii調(diào)控機制不發(fā)生損傷不發(fā)生損傷輕中度重度hypoxia-ischemiacellular energy depletioninhibition of atp dependent glu reuptakeca 2+ influx into postsynaptic cellsanaerobic glycolysis and lactate accumulationpresynaptic membrane depolarization free radical formationmitochondrial injuryglu release and activation

2、 of nmda ca 2+ channelsseveremildnecrosisapoptosis診斷側(cè)重點：1. 是否有損傷2. 損傷分級（重度 vs. 輕中度？）及范圍3. 損傷所處的階段及預(yù)后4. 鑒別診斷1time-signal curve in tii24h location of voxels and normal neonatal proton spectra. a, the deep gray nuclei voxel includes most of the lentiform nucleus, the ventrolateral thalamus, and the pos

3、terior limb of the internal capsule. the spectrum reveals: 1) a small myoinositol peak, 2) a large choline peak, 3) two small creatine/phosphocreatine peaks, and 4) a medium-sized naa peak. b, the watershed voxel includes primarily white matter from the intravascular boundary zone. note that the naa

4、 and choline peaks are relatively smaller in the less mature watershed zone than in the more mature deep gray nuclei. minimal or no lactate was seen in most patients who were developmentally normal at 12 months.neonatal asphyxia in a term neonate. short-echo-time (30 msec) (a) and long-echo-time (13

5、5 msec) (b) mr spectroscopic images obtained on day 1 of life with a voxel positioned in the right basal ganglia show a lactate (lac) doublet centered at 1.3 ppm in a and an inverted lactate doublet in b. there is also elevated glutamine-glutamate (glx) in a and low naa in b. cho choline, cr and cr2

6、 creatine resonances (3.0 ppm and 3.9 ppm, respectively).neonate with basal nuclei pattern of injury. a and b, the basal nuclei voxel (a) shows marked elevation of the lactate peak (l) centered at 1.31 ppm. in this acute phase, the relative sizes of the choline, creatine, and naa peaks are normal. the watershed voxel (b) shows less elevated lactate (compare with a)a. james barkovich, karen baranski, daniel vigneron, j. colin partridge，et al. proton mr spectroscopy for the evaluation of brain injury in asphyxiated, term neonates. ajnr 1999; 20: 1399-1405.2. benjamin y. huang, mauricio castill