The complex dynamics of stroke onset and progression

The aim of this article is to discuss the dynamic nature of cerebrovascular ischemia.

Acute risk factors are superimposed on chronic risk factors to precipitate plaque rupture in myocardial infarction. The interaction between external triggers, such as stress, with internal triggers, such as vasoconstriction, is mediated to a large part by the autonomic nervous system. Numerous algorithms have been developed to describe physiological time-series data, for example heartbeat variability, and reveal complex structure that has diagnostic and prognostic significance. Much of this structure is mediated by the autonomic nervous system. Recent data on stroke triggers, carotid stenosis, transient ischemic attack, and infarct expansion suggest a similar need for detailed physiological measurement and non-linear dynamics in order to understand stroke onset and progression.

The picture emerging is that stroke arises as a result of multiple processes with different time constants. The nature and timing of interventions should be tailored to these complex interacting processes. This will require more frequent and varied physiological measurement accompanied by non-linear analytical methods. This new approach, which stresses complex within-subject measurements, will likely make 'one size fits all' solutions to stroke care untenable.