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Arch Dis Child Fetal Neonatal Ed 1998;78:F88-F91 doi:10.1136/fn.78.2.F88
  • Special review

Hypothermic neural rescue treatment: from laboratory to cotside?

  1. A D Edwards,
  2. D Azzopardi
  1. Section of Paediatrics, Imperial College School of Medicine, Hammersmith Hospital, London
  1. Professor Edwards, Section of Paediatrics, Imperial College School of Medicine, Hammersmith Hospital, Du Cane Rd, London W12 ONN email:dedwards{at}rpms.ac.uk

    The apparent simplicity of mildly cooling the brain to lessen the devastating effects of birth asphyxia has immediate appeal to clinicians faced with the hopelessness of a severely affected infant. Many view the results of recent experimental work as encouraging. However, while researchers may spend years in the laboratory collecting results which suggest that a particular treatment shouldbe useful, it cannot be taken for granted that it will be. The scientific tools needed to demonstrate a useful biological effect are very different from those needed for accurate clinical evaluation, and investigators often need to change their focus considerably as a concept draws closer to the clinical arena.1

    Enthusiasts who would like to use moderate hypothermia to lessen brain damage after hypoxic–ischaemic or traumatic cerebral insults must now face this difficult move from laboratory to cotside. The experimental evidence is strong, but will hypothermia work in practice?

    Interpretation of experimental studies

    Many neural rescue treatments that were effective in studies of mature animals have not shown benefit in clinical trials of adult stroke patients. There is no room for complacency and laboratory results need to be interpreted with circumspection.

    First, data acquired from studies of mature animals must be treated cautiously as brain injury probably proceeds differently in the newborn and there are relatively fewer studies of hypothermic neural rescue in newborn animals. Secondly, in most experiments the delay between hypoxic–ischaemic insult and initiation of cooling has been short, and in every case clearly defined, which may not accurately reproduce the clinical situation. Furthermore, the rate of cerebral injury in the experimental control groups has been high, often 100%; it will be difficult for a clinical trial to select control groups with such high rates of severe injury, and this will make demonstration of a clinical effect more difficult. Finally, although a variety …

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