Global Hypoxic-IschaemicEncephalopathy:The brain receives 20% of cardiac output formaintaining its vital aerobic metabolism.
Numerous factors determine the mostamount of time the CNS can survive irreversible ischaemic damage. They are asunder:Ø Severity of the hypoxic episode. Ø Presence of pre-existing cerebrovascular disease.Ø Age of the patient.Ø Body temperature.Based upon the proneness of different cells ofmental performance to the consequences of ischaemia-hypoxia, three types oflesion may occur:1. Selective neuronal damage: Neurons are most susceptible to damaging effect of ischaemia-hypoxia andirreversible injury. Specifically, oligodendroglial cells are most susceptible,accompanied by astrocytes while microglial cells and vascular endotheliumsurvive the longest.
The reason behind undue vulnerability of neurons tohypoxia could be explained by various factors:Ø Different cerebral circulatory blood flow.Ø Presence of acidic excitatory neurotransmitters calledexcitotoxins.Ø Excessive metabolic requirement of the neurons.Ø Increased sensitivity of neurons to lactic acid.
2. Laminar necrosis: Global ischaemia of cerebralcortex results in uneven damage due to different cerebral vasculature whichwill be termed laminar or pseudolaminar necrosis. In this, superficial regionsof cortical layers escape damage while deeper layers are necrosed.3.
Watershed infract: Circulatory flow in mental performance by anterior, middle and posteriorcerebral arteries has overlapping circulations. In ischaemia-hypoxia, perfusionof overlapping zones, being farthest from the blood supply, suffers maximumdamage. This results in wedge-shaped regions of coagulative necrosis calledwatershed or borderzone infarcts. Particularly vulnerable could be the borderzone of the cerebral cortex between the anterior and middle cerebral arteries,producing para-sagittal infarction.
Cerebral InfarctionCerebral infarction is really a localised areaof tissue necrosis brought on by local vascular occlusion—arterial or venous.Occasionally, it may be the results of non-occlusive causes such as compressionon the cerebral arteries from outside and from hypoxic encephalopathy. Clinically,the signs and symptoms connected with cerebral infarction depend upon theregion infarcted.
1. Arterial occlusion. Occlusionof the cerebral arteries by either thrombi or emboli is the most frequentreason behind cerebral infarction.
Thrombotic occlusion of the cerebralarteries is most often the consequence of atherosclerosis, and rarely, fromarteritis of the cranial arteries. Embolic arterial occlusion is commonlyproduced from the center, most often from mural thrombosis complicatingmyocardial infarction, from atrial fibrillation and endocarditis. The size andshape of an infarct are determined by the extent of anastomotic connectionswith adjacent arterial branches as under:Ø Circle of Willis provides a complete collateral flow for internalcarotid and vertebral arteries.Ø Middle and anterior cerebral arteries have partial anastomosis ofthese distal branches. Their complete occlusion might cause infarcts.
Ø Small terminal cerebral arteries, on the contrary, are endarteriesand haven’t any anastomosis. Hence, occlusion of those branches will invariablyresult in an infarct. 2. Venous occlusion: Venous infarction inmental performance is definitely an infrequent phenomenon as a result of goodcommunications of the cerebral venous drainage. However in cancer, as a resultof increased predisposition to thrombosis, superior sagittal thrombosis mayoccur ultimately causing bilateral, parasagittal, multiple haemorrhagicinfarcts.
3. Non-occlusive causes. Compression of the cerebral arteries fromoutside such as for example occurs during herniation may cause cerebralinfarction. Mechanism of watershed (border zone) cerebral infarction in hypoxicencephalopathy had been explained above. Regardless, the extent of damageproduced by any of the above causes is determined by:Ø rate of reduced total of blood flow;Ø kind of blood vessel involved;Ø extent of collateral circulation.