Abstract
Secondary brain damage is tissue injury that is not apparent immediately after an insult, but develops after a delay of hours or days and has typically been observed after ischemia, trauma or subarachnoidal haemorrhage [1]. Secondary ischemic brain damage develops as a consequence of: (a) brain edema, (b) post-ischemic microvascular stasis and vasomotor/hemodynamic deficits leading to hypoperfusion, and (c) post-ischemic inflammation involving activation of microglia and brain infiltration of peripheral inflammatory cells [1–3]. It is believed that damage to the tissues surrounding the ischemic core, known as the penumbra, can be reduced by therapeutic measures designed to prevent or minimize molecular events contributing to the development of secondary brain damage [3].
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