A model based on the Pennes bioheat transfer equation is valid in normal brain tissue but not brain tissue suffering focal ischaemia.

Ischaemic stroke is a major public health issue in both developed and developing nations. Hypothermia is believed to be neuroprotective in cerebral ischaemia. Conversely, elevated brain temperature is associated with poor outcome after ischaemic stroke. Mechanisms of heat exchange in normally-perfused brain are relatively well understood, but these mechanisms have not been studied as extensively during focal cerebral ischaemia. A finite element model (FEM) of heat exchange during focal ischaemia in the human brain was developed, based on the Pennes bioheat equation. This model incorporated healthy (normally-perfused) brain tissue, tissue that was mildly hypoperfused but not at risk of cell death (referred to as oligaemia), tissue that was hypoperfused and at risk of death but not dead (referred to as penumbra) and tissue that had died as a result of ischaemia (referred to as infarct core). The results of simulations using this model were found to match previous in-vivo temperature data for normally-perfused brain. However, the results did not match what limited data are available for hypoperfused brain tissue, in particular the penumbra, which is the focus of acute neuroprotective treatments such as hypothermia. These results suggest that the assumptions of the Pennes bioheat equation, while valid in the brain under normal circumstances, are not valid during focal ischaemia. Further investigation into the heat exchange profiles that do occur during focal ischaemia may yield results for clinical trials of therapeutic hypothermia.