Global encephalopathy. Clinically, the signs and symptoms

Global Hypoxic-Ischaemic
Encephalopathy:

The brain receives 20% of cardiac output for
maintaining its vital aerobic metabolism. Numerous factors determine the most
amount of time the CNS can survive irreversible ischaemic damage. They are as
under:

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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 of
mental performance to the consequences of ischaemia-hypoxia, three types of
lesion may occur:

1. Selective neuronal damage:

            
Neurons are most susceptible to damaging effect of ischaemia-hypoxia and
irreversible injury. Specifically, oligodendroglial cells are most susceptible,
accompanied by astrocytes while microglial cells and vascular endothelium
survive the longest. The reason behind undue vulnerability of neurons to
hypoxia could be explained by various factors:

Ø 
Different cerebral circulatory blood flow.

Ø 
Presence of acidic excitatory neurotransmitters called
excitotoxins.

Ø 
Excessive metabolic requirement of the neurons.

Ø 
Increased sensitivity of neurons to lactic acid.

 

 

 

2. Laminar necrosis:

             Global ischaemia of cerebral
cortex results in uneven damage due to different cerebral vasculature which
will be termed laminar or pseudolaminar necrosis. In this, superficial regions
of cortical layers escape damage while deeper layers are necrosed.

3. Watershed infract:

             
Circulatory flow in mental performance by anterior, middle and posterior
cerebral arteries has overlapping circulations. In ischaemia-hypoxia, perfusion
of overlapping zones, being farthest from the blood supply, suffers maximum
damage. This results in wedge-shaped regions of coagulative necrosis called
watershed or borderzone infarcts. Particularly vulnerable could be the border
zone of the cerebral cortex between the anterior and middle cerebral arteries,
producing  para-sagittal infarction.

Cerebral Infarction

Cerebral infarction is really a localised area
of tissue necrosis brought on by local vascular occlusion—arterial or venous.
Occasionally, it may be the results of non-occlusive causes such as compression
on the cerebral arteries from outside and from hypoxic encephalopathy. Clinically,
the signs and symptoms connected with cerebral infarction depend upon the
region infarcted.

   1. Arterial occlusion.

              Occlusion
of the cerebral arteries by either thrombi or emboli is the most frequent
reason behind cerebral infarction. Thrombotic occlusion of the cerebral
arteries is most often the consequence of atherosclerosis, and rarely, from
arteritis of the cranial arteries. Embolic arterial occlusion is commonly
produced from the center, most often from mural thrombosis complicating
myocardial infarction, from atrial fibrillation and endocarditis. The size and
shape of an infarct are determined by the extent of anastomotic connections
with adjacent arterial branches as under:

Ø 
Circle of Willis provides a complete collateral flow for internal
carotid and vertebral arteries.

Ø 
Middle and anterior cerebral arteries have partial anastomosis of
these distal branches. Their complete occlusion might cause infarcts.

Ø 
Small terminal cerebral arteries, on the contrary, are endarteries
and haven’t any anastomosis. Hence, occlusion of those branches will invariably
result in an infarct. 

2. Venous occlusion:

                  Venous infarction in
mental performance is definitely an infrequent phenomenon as a result of good
communications of the cerebral venous drainage. However in cancer, as a result
of increased predisposition to thrombosis, superior sagittal thrombosis may
occur ultimately causing bilateral, parasagittal, multiple haemorrhagic
infarcts.

3. Non-occlusive causes.

                 Compression of the cerebral arteries from
outside such as for example occurs during herniation may cause cerebral
infarction. Mechanism of watershed (border zone) cerebral infarction in hypoxic
encephalopathy had been explained above. Regardless, the extent of damage
produced 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.