Cerebral infarction

[1] In mid to high income countries, a stroke is the main reason for disability among people and the 2nd cause of death.

[9] In recent years, a study has been done to show how AI can aid in diagnosis of cerebral infarct and improve patient outcomes in areas that may not have stroke trained physicians.

[16] Cerebral infarction is caused by a disruption to blood supply that is severe enough and long enough in duration to result in tissue death.

[21] If blood flow is reduced enough, oxygen delivery can decrease enough to cause the tissue to undergo the ischemic cascade.

A CT scan will rule out a hemorrhagic stroke, is cheaper for the patient, and can be found in almost all hospitals unlike an MRI machine.

[25] An MRI can help to diagnose an acute cerebral infarct as quickly as 6 hours from start of symptoms,[25] It can also help time when the stroke happened.

[28] A head and neck CT angiogram can be performed within 6 hours of onset of symptoms to see where the occlusion may be located which can help in determining the cause of the stroke.

The use of intravenous rtPA therapy can be advocated in patients who arrive to stroke unit and can be fully evaluated within 3 hours of the onset.

[31] In increasing numbers of primary stroke centers, pharmacologic thrombolysis with the drug tissue plasminogen activator (tPA), is used to dissolve the clot and unblock the artery.

This is accomplished by inserting a catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the clot, which is then withdrawn from the body.

[37] This data suggests that a large, randomized controlled trial is needed to more completely evaluate the possible therapeutic advantage of this treatment.

Permissive hypertension - allowing for higher than normal blood pressures in the acute phase of cerebral infarction - can be used to encourage perfusion to the penumbra.

Cerebral infarction
Hemodynamic changes seen using an IOS camera specific for hemoglobin volume changes where we see the occlusion of a Middle Cerebral Artery (MCA) and how Spreading Depolarizations appear and spread over the cortex. [ 11 ]
Histopathology at low magnification of a cerebral infarction on H&E stain , showing pallor in the infarcted area due to edema.
Histopathology at high magnification of a normal neuron, and a cerebral infarction at approximately 24 hours on H&E stain : The neurons become hypereosinophilic and there is an infiltrate of neutrophils . There is slight edema and loss of normal architecture in the surrounding neuropil .