With the advent of non-invasive imaging evidence has been provided that brain infarcts grow. This growth is not due to the progression of ischemia because the activation of collateral blood supply and spontaneous thrombolysis tend to improve blood flow over time. Infarct progression can be differentiated into three phases. During the acute phase tissue injury is the direct consequence of the ischemia-induced energy failure and the resulting terminal depolarization of cell membranes. At flow values below the threshold of energy metabolism this injury is established within a few minutes after the onset of ischemia. During the subsequent subacute phase, the infarct core expands into the peri-infarct penumbra until, after 4-6 hours, core and penumbra merge. The reasons for this expansion are peri-infarct spreading depressions and a multitude of cell biological disturbances, collectively referred to as molecular cell injury. Finally, a delayed phase of injury evolves which may last for several days or even weeks. During this phase secondary phenomena such as vasogenic edema, inflammation and possibly programmed cell death may contribute to a further progression of injury.
The largest increment of infarct volume occurs during the subacute phase in which the infarct core expands into the penumbra. Using multiparametric imaging techniques for the differentiation between core and penumbra, evidence could be provided that 1 hour after occlusion of the middle cerebral artery the penumbra is still approximately of the same size
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