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Hemorrhagic Infarct
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Hemorrhagic Infarct

A coronal section through the brain at the level of the caudate nucleus and putamen.
The arrow points to hemorrhagic infarction of the putamen and caudate nucleus.
The overlying cerebral cortex and white matter is also involved but the hemorrhagic part of a hemorrhagic infarct is usually confined to the grey matter.
Note how swollen the affected hemisphere is, with herniation of structures across the midline.
Most hemorrhagic infarcts are due to emboli.
(Description By:Margaret Grunnet,M.D. )
(Image Contrib. by: UCHC )
Infarct
Etiology

Cerebral infarcts are due to occlusion of an artery by a thrombus or embolus effectively cutting off nutrients and oxygen to the area fed by the artery.
Pathogenesis

The most comman cause of cerebral infarct is due to atherosclerosis of cerebral and coronary arteries which is related to age, smoking, hypertension, serum lipids and cholesterol, and diabetes.,
Epidemiology

Stroke is a common cause of death and disablility in patients over 55 but can be seen younger individuals as well.
General Gross Description

The brain shows tannish discoloration and swelling as well as softening in the area of the pale infarct.
In the hemorrhagic infarct, the grey matter will show multiple petechial hemmorrhages in the area affected.
General Microscopic Description

Microscopically, the cerebral grey and white matter in the affected area will be pale show vacuolization at the border between the infarct and intact tissue.
Within the first 24 hours, a few neutrophils will appear.
Within three days, macrophages will appear to phagocytose necrotic tissue and there will be swelling or reactive change in astrocytes at the border of the infarct as if to wall it off.
Clinical Correlation

Patients with a cerebral infarct (stroke) will have the sudden onset of focal neurological deficit such as a hemiparesis which gets somewhat worse with the accompanying edema and then stabilizes, unless there has been a massive stroke with edema, herniation and death.
After beginning resolution of the infarct, the patients neurological deficit may improve.
References

Cotran RS, Kumar V, Robbins SL: Robbins Pathologic Basis of Disease. 5th ed. Philadelphia, W.B. Saunders, 1994, pp. 1309-1311.
Poirer J et.al. Manual of basic neuropathology. Philadelphia: Saunders, 1990, pp. 79-92.
Infarct
Synopsis by: M.L. Grunnet M.D. (TX2000M54700)[62]
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