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Mod03Slide24-25

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Module: 3 Slide: 24

Description: Brain Stem Infarct

 

 

Slide Description: This brain stem shows a recent infarct, into which hemorrhage has occured. Hemorrhage into the brain may occur with rupture of a vessel, but here the hemorrhage is presumably due to bleeding from vessels in and adjacent to the soft, liquefied necrotic tissue.

 

IMDEPSAASIAC:

Identify: cross sxn of brain stem

 

Morphology: Recent infarct with hemorrhage

 

Disease: brain stem infarct

 

Etiology (main): Occlusion of a branch of the basilar artery.

 

Pathogenic mechanism: Infarctions in the brain stem are usually caused by atherosclerosis with superimposed thrombosis.

 

Structural changes (specific, gross, and micro): Early in a cerebral infarct we see swelling and softening of the necrotic tissue. Within 3 days there is infiltration of macrophages which consume the necrotic tissue. By 1 months there is continued phagocytosis of tissue and liquefaction of the infarct. By 6 months the infarct has completely liquefied.

 

Are there any other sites of involvement in the body?

 

Are there any other diseases where similar changes can be seen? Staphylocoocal infection, cryptococcus, Toxoplasmosis, Cystercercosis,

 

Signs / Symptoms: Dependent on location.

 

Investigations (confirmation / gauge extent): MRI

 

Are there any other diseases you have studied where such tests can be positive?

 

Course of disease progress (complications, monitoring, outcome): TIAs to death if involving the reticular formation.

 

Lab Questions:

 

1. What is the common cause of infarction of the brain?

Cerebral atherosclerosis is the most common cause of brain infarcts, and factors that predispose individuals to atheroscleosis (smoking, diabetes, hypertension) increase the risk of infarcts.

 

2. How do brain infarcts heal?

38 to 48 hoursThe necrotic area becomes swollen and softer with interstitial and intracellular edema. Areas of hemorrhage may be seen.
3rd dayMacrophages begin to inflitrate the lesion and phagocytose necrotic parenchyma (Gitter cells) resulting in progressively sharper demarcation of the infarct.
1 monthExtensive phagocytosis of necrotic parenchyma results in further softening and liquefaction of the infarct.
6 monthsInfarct is completely liquefied leaving behind a permanent, fluid-filled, cystic defect in place of the tissue with a surrounding region of gliosis.

 

 

Vignette

A 58 year old male with poorly controlled hypertension presents to the ER with right-sided hemiparesis, spasticity, and aphasia. His wife tells you that he quit smoking only 3 months prior. His medical record shows 3 previous episodes of transient ischemic attacks within the past 4 years and all were self-limiting. Given his history and presenting symptoms you make the tentative diagnosis of a left-sided cerebral infarct with occlusion of a branch of the middle cerebral artery.


 

 

Module: 3 Slide: 25

Description: Foam cells

 

 

Slide Description: Phagocytic cells have entered an area of cerebral infarction. There cells, also a part of the monoyte/macrophage system, are derived in part from the microglia and in part from monocytes of the blood that transform into macrophages when they leave the vascular system. These cells engulf the liquefied material, and they may be known then as "foam cells", as their cytoplasm becomes filled with lipid material. Processing of the tissue for slides dissolves this, leaving a pale, "bubbly" cytoplasm.

 

Lab Questions:

 

1. How can you age an infarct?

By looking at the gross morphology and histology of an infarct you can gauage the relative age of it. Infarcts within 48 hours swollen and softer with interstitial and intracellular edema. Areas of hemorrhage may be seen. By day 3 there is macrophage infiltration of the infarct and progressively sharper demarcation of the infarct on gross examination. By 1 month there is extensive phagocytosis and liquefaction of the infarct. By 6 months there is total liquefaction of the infarct, leaving a fluid filled cyst.

 

2. Why do the cells here appear foamy?

These macrophages are consuming necrotic brain tissue which is highly myelinated, hence full of lipids. On processing of the slide the alcohol used to prepare the slide washes out the fatty contents of the macrophages causing them to appear foamy.

 

 

3. How long does it take for brain cell to die after occlusion to an atery.

Cell death occurs within minutes of arterial occlusion although the gross and histologic appearance of the brain is normal for up to 12 hours.

 

4. What are foam cells? By what other name are they known?

Foam cells are microglia (macrophages of the CNS). In the context of tissue necrosis when microglia accumulate an abundant amount intracellular lipid they are also known as Gitter cells.

 

5. What other cell types may be found in the CNS?

Astrocytes --> Major supporting cells in the brain. In response to parenchymal injury, astrocytes respond by producing a dense network of processess similar to a fibrous scar.

Oligodendrocytes -->Analogous to Schwann cells in the PNS.

Ependymal cells --> Line the cerebral ventricle and are cloesly related to the cuboidal cells that invest the choroid plexus.

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