was 0.37 (SD 0.76) and the mean Z-score for motor out-come was 0.67 (SD 0.88). No differences were found in neurodevelopmental and motor outcome between pa-tients with no/mild white matter abnormalities and pa-tients with moderate-to-severe white matter abnormal-ities. There were no differences between the two Hb con-centration groups for the neurodevelopmental outcome In this retrospective study we were able to show that lesions in the basal ganglia and thalami, and especially in the white matter, are common findings in infants with severe neonatal anaemia. Cerebral damage has been suggested to be caused by several pathophysiological mechanisms. In full-term in-fants, the deep grey matter nuclei are probably affected after an acute hypoxic-ischaemic insult due to changes in brain maturation and increased metabolic demands [1]. White matter injury is also found in full-term infants and is considered to be due to more prolonged and repetitive hypoxic-ischaemic events. A combination of deep grey matter damage and white matter lesions can also be found [2]. We hypothesize that the mechanisms that cause bas-al ganglia and white matter injury following severe anae-mia might be similar to the mechanisms responsible for cerebral injury in full-term infants with perinatal asphyx-ia due to other causes. White matter injury has been de-scribed in animals as well as in humans after moderate prolonged foetal or neonatal asphyxia, as well as after neonatal hypoglycaemia [3, 4]. It is important to note that a substantial percentage (31%) of our anaemic patients also had a period of hypoglycaemia. The mechanism of injury due to hypoglycaemia is still unclear, although it has been hypothesized that it is caused by increased re-gional cerebral blood flow during hypoglycaemia with a subsequent reduction in regional glucose uptake [3]. Even more interesting are the clinical implications of these findings. MRI is a well-established method to as-sess brain injury in infants suffering from perinatal as-phyxia, and these findings are closely related to later neurodevelopmental outcome [5–11]. Data on the long-term outcome of patients with severe acute anaemia combined with a less severe component of perinatal as-phyxia are still limited. It is of interest that early neuro-developmental and motor outcomes in the first 2 years of life in the survivors is favourable. In the absence of damage in the thalamus and basal ganglia, neonatal anaemia itself does not have a significant effect on out-come at 2 years of age [12]. However, the children are still young and their outcome should be re-assessed at school age. We also found that the severity of anaemia does not influence the need for intensive care treatment in the neonatal period. Moreover, we also found that there was no significant difference in survival between patients with an initial Hb concentration ≤3.0 mmol/l versus patients with an initial Hb concentration between 3.1 and 6.0 mmol/l. There was also no increased need for respiratory or circulatory support in the infants with more severe anaemia. However, the degree of organ fail-ure and especially the degree of encephalopathy scored clinically or with aEEG and the presence of seizure activ-ity and severe injury on MRI were correlated with mor-tality and/or redirection of care. Limitations This retrospective study has several limitations. First, Hb concentrations were not assessed within a predefined time after birth. However, all Hb measurements were per-formed within 6 h after birth, indicating severe neonatal anaemia. Second, MRI imaging was initially restricted to infants with a clinical indication, although MRI was also performed in patients with anaemia without serious co-morbidity. Although this may have caused a potential bias, clinical characteristics in infants with and without MRI data were not different. Third, a full neurodevelop-mental assessment was not performed routinely. It would therefore be desirable to have a follow-up in these patients at school age to study whether the white matter lesions are associated with school performance, as has previously been shown in survivors with white matter injury in the context of hypoxic ischaemic encephalopathy [13]. More insight in the association between patterns of damage and possible pathophysiological mechanisms, combined with neurological outcome, will hopefully provide more in-sight in how to predict future disabilities during the new-born period. Severe neonatal anaemia is associated with high neo-natal mortality and neonatal morbidity. Those who sur-vive perform relatively well when assessed at approxi-mately 2 years of age. MRI shows abnormalities in the basal ganglia and thal-ami in severely affected infants, and white matter lesions in most patients. However, it is difficult to distinguish between damage due to anaemia only and damage due to associated perinatal asphyxia. Due to the retrospective setup of this study and miss-ing data, results should be interpreted with caution. Pro-spectively collected data with a longer follow-up period are needed.Posterior limb of internal capsule: 0 = normal, 1 = reduced or asymmetrical signal intensity, and 2 = severe injury with reversed or abnormal signal intensity bilaterally on T1- and or T2-weighted images.Basal ganglia and thalami: 0 = normal, 1 = mild injury (focal abnormal signal intensity), 2 = moderate injury (multifocal abnor-mal signal intensity), and 3 = indicates severe injury (widespread abnormal signal intensity).White matter: 0 = normal, 1 = mild injury (long T1 and T2 in periventricular white matter only), 2 = long T1 and T2 in subcorti-cal WM and or focal punctate lesions or focal infarction, and 3 = severe widespread abnormalities including long T1 and T2, infarc-tion, and haemorrhage. Cortex: 0 = normal, 1 = mild (1–2 sites cortical highlighting/ decreased T1), 2 = moderate (3 sites involved) and 3 = severe (>3 sites). 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