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Cerebral and systemic pathophysiological responses to acute stroke.

The concept of a systemic pathophysiological response to cerebral damage was first developed nearly 150 years ago by Claude Bernard. In one of his experiments he demonstrated that an artificially induced lesion in the floor of the fourth ventricle of a rabbit produced a peripheral hyperglycaemic response [1]. There are now known to be many cellular and molecular responses to acute cerebral injury. Some cellular responses to cerebral ischaemia occur within 15 s in animal stroke models [2]. Increased catabolic hormone release probably occurs within a few minutes, while the cardiovascular responses such as changes in blood pressure (BP) are well established within 20 min [3]. However, other responses such as the cerebral inflammatory response only begin after 20–24 h, while changes in bone mineral density in the hemiplegic limbs take many weeks to develop [4, 5]. Therefore, although most metabolic responses are initiated rapidly, other pathophysiological changes persist and continue to develop after the acute phase.