Kim Annink

256 Chapter 12 similar to ulegyria in the cerebrum (22). The reason for this distribution is unknown. One hypothesis is that because the arterial ramifications of the more peripheral arteries at the bases of the sulci have a smaller diameter, the Purkinje cells there are more susceptible to hypoxic-ischemia (23–25). Recently, Wright et al. described 23 children in whom MRI abnormalities were seen in the bases of the sulci of the cerebellar hemispheres after hypoxic-ischemic events (26). This injury was especially located at the borderzones of cerebellar artery territories and associated with supratentorial watershed injury, therefore they called it cerebellar watershed injury (26). This study underlines our pathological finding that Purkinje cells at the bases of the sulci in the vermis are more susceptible to hypoxia compared to the crowns in neonates with HIE and the hypothesis that this is probably caused by impaired perfusion of the bases of the sulci. The clinical significance should be investigated in the near future as well as the existence of a similar pattern of Purkinje cell injury in the cerebellar hemispheres. It would be interesting to investigate whether this pattern is visible at school-age on MRI and how it effects long-term outcome. Chapter two confirms that cerebellar injury is detectable with postmortem histopathology; the next question was whether cerebellar injury is visible on MRI. Others published that using conventional imaging, cerebellar injury is very difficult to visualize, but more quantitative methods might reveal more details (27,28). In chapter three , we compare cerebellar injury confirmed with histopathology to apparent diffusion coefficient (ADC) values on diffusion-weighted MRI (DWI) in infants with HIE. Infants with congenital non-cardiac anomalies requiring neonatal surgery, with normal postoperative MRI’s and normal two year outcome served as controls. ADC values in the vermis and dentate nucleus were significantly lower in infants with HIE compared to the patients without brain injury. ADC values in the cerebellar hemispheres did not differ. When we compared ADC values with histopathology in the infants with HIE, ADC values in the cerebellar vermis in infants with HIE were significantly correlated with Purkinje cell injury. ADC values did not differ in patients with mild and severe inflammation or histopathological cytotoxic edema. So it is important to realize that, even when the DWI seems to be normal and the ADC values are within the normal range, there still might be cerebellar injury. The ADC values in the vermis are most representative for cerebellar injury. Though MRI might underestimate cerebellar injury, it is an accurate biomarker for brain injury in infants with HIE and the gold standard for neuroimaging. For