Pathology Review Carousel 11
Neuropathology II



Image

Slide #

Tissue

Mag

Feature

1

Brain

Gross

Purulent Meningitis. A creamy or yellow-white exudate opacifies the leptomeninges.

2

Brain

LP

Purulent Meningitis. The subarachnoid space is filled with cells and the blood vessels are congested.

3

Brain

HP

Purulent Meningitis. Closer view of predominantly neurtophilic infiltrate.

5

Hippocampus

LP

Acute Hemorrhagic Infarct. Note the curved row of closely spaced nuclei of granuel cells of the dentate gyrus. At this magnification only the disruption of tissue by recent hemorrhage can be identified.

6

Hippocampus

MP

Acute Hemorrhagic Infarct. Recent hemorrhage, and some eosinophilia of neurons can be noted.

7

Hippocampus

HP

Acute Infarct. Note eosinophilic neurons (coagulation necrosis).

8

Cerebrum

Gross

Hemorrhagic Infarct. There is necrosis in addition to the hemorrhage. (In general results from embolic occlusion). Distribution of middle cerebral artery. (Infarct of end-arterial zone).

9

Cerebrum

Gross

Anemic Infarct. (In general from in situ thrombotic occlusion).

10

Cerebrum

Gross

Thrombosis of the superior sagittal sinus with bilateral hemorrhagic infarcts.

11

Cerebrum in horizontal section with watershed infarcts.

Gross

Multiple foci of necrosis from global ischemia such as hypotension or cardiac arrest. Watershed areas, hippocampus and cerebellum are areas most vulnerable.

13

Hippocampus

LP

Area of old ischemic injury showing Sommer's sector neuronal vulnerability to ischemia. Sommer's sector is the region of the pyramidal cell layer near the sharp curve of the dentate gyrus.

14

Hippocampus

MP

Same. Note loss of pyramidal neurons from Sommer's sector.

16

Cerebrum

MP

Old, cavitated infarct. Because the brain has so little protein, it undergoes liquefactive necrosis. Note persistence of the molecular layer which differentiates this from an old contusion.

17

Cerebrum

HP

Old, cavitated infarct. Gitter cells or macrophages (large cells with foamy cytoplasm) fill the cavity to remove debris, leaving only thin-walled blood vessels.

18

Cerebrum

LP

Old, cavitated, laminar necrosis. Laminar necrosis often follows hypotension of relatively slow onset but of long duration. Again note persistence of molecular layer and involvement at the base of a sulcus indicating the lesion is ischemic in nature and not a contusion.

19

Cerebrum

MP

cavity of the cavitated laminar necrosis with gitter cells and thin walled blood vessels.

20

Cerebrum

HP

Reactive or gemistocytic astrocytes (plump cells with abundant eosinophilic cytoplasm) at periphery of old infarct.

21

Cerebrum

Gross

Laminar necrosis with early cavitation. Note persistence of the outer most gray matter.

22

Cerebrum

Gross

Old, cavitated infarct in the distribution of the anterior cerebral artery. Note the infarct was complete.

23

Cerebrum

Gross

Lacunes. Small cavitary infarcts, resulting from hypertension, most frequently involving the basal ganglia (caudate nucleus, globus pallidus, putamen, and amygdala) and basis pontis. Compare right with left.

24

Basal ganglia

Gross

Same. Note the small (0.2-15 cu mm) cavities.

26

Cerebral cortex

MP

Alzheimer's disease. Congo Red stain. Note orange staining neuritic plaque orange and congophilic angiopathy.

27

Cerebral cortex

MP

Alzheimer's disease. Note eosinophilic staining of the amyloid deposited in an daround the vessel wall (congophilic angiopathy). With congo red stain the vessel would appear orange.

28

Cerebral cortex

HP

Alzheimer's disease. Neuritic or senile plaque consisting of central core of extracellular amyloid (stains orange) surrounded by degenerating neuritic terminals and reactive microglia and astrocytes.

29

Cerebral cortex

MP

Alzheimer's disease. Congo red stain with polarized light.

30

Cerebral cortex

HP

Alzheimer's disease. Silver stain. Within neurons note the bundles of black staining neurofibrillary tangles. Ntoe the senile or neuritic plaque which appears as a tangled ball of black staining dystrophic neuritic processes.

31

Cerebral cortex

Very HP

Alzheimer's disease. Neuron iwth granuolo-vacuolar degeneration (cytoplasmic black dots surrounded by small halo).

32

Brain

Gross

Alzheimer's disease. Hydrocephalus ex vacuo (compensatory expansion of the ventricles due to atrophy of the brain and can occur with severe cases of Alzheimer's disease). Also note narrowed gyri and wide sulci in some areas.

34

Meninges

HP

Cryptococcal meningitis. Mucicarmine stains cryptococcal capsule red. Note scant inflammatory response with mononuclear inflammatory cells (lymphocytes and macrophages).

35

Brain

LP

Viral encephalitis. At this power note the perivascular cuffing and the cellularity of the adjacent brain parenchyma.

36

Brain

MP

Same. The perivascular cells can be recognized as mononuclear inflammatory cells.

37

Brain

MP

Same.

38

Gray matter

HP

Viral encephalitis. Microglial nodule (formed by hyperplasia and proliferation of "microglial cells") near degenerating neurons.

39

Gray matter

HP

Same. One neuron iwth its large pale nucleus and distinct nucleolus is undergoing neuronophagia (destruction of a nuron by the phagocytic process).


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