Cooling the Preterm Brain

There is now strong clinical and experimental evidence that prolonged, moderate cerebral hypothermia initiated within a few hours after severe hypoxia-ischaemia and continued until resolution of the acute phase of delayed cell death can reduce subsequent neuronal loss and improve behavioral recovery (1-8). However, these studies have focused on neuroprotection for term infants and in adults. Preterm infants have a very high burden of neurological injury and subsequent neurodevelopmental handicap including overt cerebral palsy and cognitive and learning deficits. Although the etiology of brain injury in premature infants is complex and multifactorial, there is considerable evidence linking injury with exposure to hypoxia and cerebral ischemia, particularly at birth and in the first few days of life. Indeed, larger premature infants, from 31 to 36 gestation, with metabolic acidosis on umbilical cord blood samples have a high rate of clinical encephalopathy and subsequent basal ganglia damage, and thus, may be candidates for experimental neuroprotective treatments (9). Nevertheless, direct translation of therapeutic to the preterm infant is problemati