Hypothermia decreases the cerebral metabolic rate for glucose and oxygen and reduces the loss of high energy phosphates during ischaemia and prevents or ameliorates secondary cerebral energy failure

Experimental evidence of the value of post-insult cooling Studies of mild hypothermia for neural rescue after perinatal asphyxia commenced when experimental studies in animals suggested that mild hypothermia applied soon after hypoxia-ischaemia lessened pathophysiological abnormalities and improved functional outcome . Several studies confirmed that post-insult cooling reduced injury in immature animals . The mechanism of protection is unclear, but hypothermia attenuates blood brain barrier damage; release of excitatory neurotransmitters is reduced; free radical production is lessened and IL-10 (an anti-inflammatory cytokine) is increased . Hypothermia decreases the cerebral metabolic rate for glucose and oxygen and reduces the loss of high energy phosphates during ischaemia and prevents or ameliorates secondary cerebral energy failure . Importantly, hypothermia influences apoptotic mechanisms within cells: caspase 3 activity is lessened and cytochrome c translocation is diminished, resulting in a reduction in apoptotic neurons 14. Following global hypoxic or HI or traumatic insults mild hypothermia reduces damage in the cortex, thalamus and hippocampus. Treated animals also demonstrate preserved neurological functions. Although some of these benefits may diminish over time, the protection provided by post-insult hypothermia generally persists .