Cerebral palsy (CP) is caused by either hypoxia-ischemia (H-I) or long-standing causative factors such as inflammation or genetics. Multiple pathophysiological events over time are thought to contribute eventually to cerebral palsy. Our objective was to examine whether the immediate response of the fetus to an acute H-I event determined the motor deficits associated with cerebral palsy.


Serial diffusion-weighted imaging were performed on 79% gestation New Zealand white rabbits using a 3-Tesla magnetic resonance scanner during 40 minutes of uterine ischemia, 20 minutes of reperfusion, and at 4, 24, and 72 hours. Individual fetuses were tracked to near term, and the delivered kits were divided into hypertonic H-I (n = 18), nonhypertonic H-I (n = 9), stillbirth H-I (n = 4), and control groups (n = 16).


The hypertonia group had significantly less of a nadir in apparent diffusion coefficient (ADC) during H-I (71.6 ± 23.8% vs 84.5 ± 9.3% baseline) and slower and incomplete recovery of ADC during reperfusion compared with the nonhypertonic group. All fetuses in the hypertonic and stillbirth groups had an ADC nadir of less than 0.83μm2/msec (70.3% decrease from baseline), whereas 94% of control animals had an ADC nadir greater than this value. The difference between outcome groups was the largest at 4 hours reperfusion and persisted for 24 hours.


Serial fetal brain scans indicate that the immediate response of a fetus to H-I is crucial to the development of hypertonia. If the fetal brain can be scanned at the time of insult, ADC changes can predict which fetuses will have an unfavorable outcome. Ann Neurol 2007;61:307–314