Infarction
The arteriolar sclerosis that results from chronic hypertension leads to small lacunar infarcts, or "lacunes", one of which is seen here in the pons. Such lesions are most common in basal ganglia, deep white matter, and brain stem.
This is the microscopic appearance of a lacunar infarct. Note that it is a cystic space from the resolved liquefactive necrosis. There can be hemosiderin pigment from hemorrhage as well.
An acute cerebral infarct is seen here. Such infarcts are typically the result of arterial thrombosis or embolism.
This is an intermediate to remote infarct in the distribution of the middle cerebral artery
A thrombosis of the internal carotid artery is seen here. Arterial thromboses are far more common in the brain than venous thromboses (by a ratio of about 100 to 1
Thromboemboli can lodge in cerebral arteries, particularly in the distribution of the middle cerebral, and peripherally toward branch points. Here is a thromboembolus that originated from mural thrombus in the left atrium. The heart is a common source for such emboli.
This intermediate infarct of the frontal lobe shows liquefactive necrosis with formation of cystic spaces as resolution begins
Here is a cerebral infarct from an arterial embolus, which often leads to a hemorrhagic appearance. There is edema which obscures the structures. The acutely edematous infarcted tissue may produce a mass effect. Note the decrease in size of the ventricle on the left with shift of the midline.
The microscopic appearance of this acute cerebral infarction reveals marked edema (the pale areas).
The neurons are the most sensitive cells to anoxic injury. Seen here are red neurons which are dying as a result of hypoxia.
The Purkinje cells between the molecular and granular layers of the cerebellum are also highly susceptible to anoxia. Those seen here are red.
The subacute (intermediate) infarct seen here at the right shows edema with obscured structural outlines and swelling that shifts the midline to the left. There is liquefactive necrosis with beginning formation of cystic spaces.
This cerebral infarction demonstrates the presence of many macrophages at the right which are cleaning up the lipid debris from the liquefactive necrosis.
Here is a large remote cerebral infarction. Resolution of the infarction has left a huge cystic space encompassing much of the cerebral hemisphere in this neonate
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Edema and Herniation
There is cerebral edema seen at the right which obscures the structures. There is a shift of the midline to the left. Multiple small metastases were the cause for the edema in this case.
The surface of the brain with cerebral edema demonstrates widened gyri with a flattened surface. The sulci are narrowed
Acute brain swelling in the closed cranial cavity is serious. Swelling of the left cerebral hemisphere has produced a shift with herniation of the uncus of the hippocampus through the tentorium, leading to the groove seen at the white arrow. |
The end result of temporal medial lobe herniation is compression of the brainstem (midbrain and pons) and stretching of small arterial branches to cause Duret hemorrhages, as seen here in the pons.
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