- 
The brain tissue undergoing ischemia has two distinct layers, an internal core layer of ischemic cells with blood perfusion less than 10-25%, which illustrate the death of different types of neural cell. The second layer is an external layer that has underwent a lesser ischemic process (penumbra) that is the target of therapy for achieving functional recovery. After ischemic stroke attack, the centre of the core layer is perfused at 10-12 ml/100g/min or fewer, in contrast, the ischemic area surrounding it critically hypo-perfused at fewer than 18-20 ml/100g/min and is at risk of irreversible tissue damage. While the penumbra is perfused at less likely at about 60 ml/100 g/min and less likely to undergo immediate complete irreversible tissue destruction. However,this tissue may be recovered again if it is re-perfused in a certain time window.
3. The effect of brain edema
This concept plays a major role in the prognosis of stroke patients. Cytotoxic edema could develop and progress within minutes to hours following ischemia and is landmarked by the brain tissue swelling. Malignant middle cerebral arteria infarctions are defined by the space occupying edema caused.
4. Effects of ischaemic stroke on the structural integrity of the cerebral tissue
Brain cells hypoxia resulting in disruption of the blood vessel integral structure leads to interrupting in the blood-brain barrier. Many studies have shown that ischemia can cause alterations to blood vessels endothelin receptors.
To summarize:
Understanding of the above procedures is crucial to saving brain tissue and saving lives. Brain tissue undergoing ischemic process could be saved during the first hours by reperfusion methods available in the hospitals.
References:
1. P.U. Heuschmann, K. Berger, B. Misselwitz, P. Hermanek, C. Leffmann, M. Adelmann, H.J. Buecker-Nott, J. Rother, B. Neundoerfer, P.L. Kolominsky-Rabas, Frequency of thrombolytic therapy in patients with acute ischemic stroke and the risk of in-hospital mortality: the German Stroke Registers Study Group, Stroke 34 (2003) 1106–1113.
2. I. Klatzo, Pathophysiological aspects of brain edema, Acta Neuropathol. (Berl.) 72 (1987) 236–239.
3. R.A. Fishman, Cerebrospinal Fluid in Diseases in the Nervous System, 2nd Ed., W.B. Saunders Co., Philadelphia, PA, 1992, pp. 103–155.
4. L. Edvinsson, Cerebrovascular endothelin receptor upregulation incerebral ischemia, Curr. Vasc. Pharmacol. 7 (2009) 26–33.”
Written by Burhan Fakhurji
