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Flashcards in Neuropathology III Deck (21):
1

What do the lenticulostriate arteries supply? From what are they derived?

from middle cerebral arteries
supply striatum and posterior limb of the internal capsule. this is an "end" artery

2

What do superficial branches supply? How are they organized? What are the implications for infarcts/hypotension?

go to the surface of the brain and provide overlapping collateral circulations/anastamoses. Area between 2 contiguous territories of blood supply is a watershed area/border zone.
In an occlusion setting, this may be protective. However, in sudden pressure drops (shock), these areas are most vulternable to ischemia.

3

What characterizes borderzone infarctions caused by sudden loss of perfusion pressure?

loss of neurons in an uneven distrubution. Preservation of some layers and loss of others- pseudolaminar necrosis.

4

What is subclavian steal syndrome?

vertebral and brachial arteries are related. if you occlude the suclavian artery proximal to the vertebral artery, or if you exercise the brachail artery too vigorously, you may steal blood from brain. (on the right side)

5

Where are emboli most common?

distribution of the MCA. lodge at the origin or trifuration.

6

What are the sources of emboli? Include specific sources from the heart.

ulcerated plaques in large vessels
in the heart:
1. atrial clots in pts with a-fib
2. mural thrombi from MIs
3. vegetation on valves or prosthesis

7

To what conditions might cholesterol emboli be secondary?

surgical manip of atheromtous aorta
invasive neuro procedures
anticoagulants of pts with advanced atherosclerosis.

8

Where do septic embolic usually go and what do they cause?

lodge in peripheral arterial branches and cause inflammation and vessel destruction. may also destroy the cell wall, or result in aneurysmal dilation with risk of hemorrhagic rupture.

9

What is the ischemic cascade that leads to damage?

1. Ischemia leads to anaerobic metabolism
2. anaerobic metabolism leads to lactic production
3. Absence of ATP leads to failure of ATP dependent Ca pumps
4. Without CA pumps, Ca flows into the cell.
4. Ca causes glutamate release
5. Glutamate interacts with NMDA receptors and makes them more excitable.
6. Excitotoxicity leads to the release of free radicales, proteases, and more glutamate
7. all of this causes cell destruction (membrane breakdown, mitochondrial damage and apoptosis). Inflammatory response beigns

10

What happens after cerebral infarction (what develops)? What are the types of infarction?

area of softening: ecephalomalacia). This is tissue necrosis and involves all elements (neurons, glia, vessels)
ischemic (aka pale) vs hemorrhagic

11

What are main causes of large, medium, and small infarcts, respectively? What causes watershed infarcts?

large: thombi/emboli
medium: emboly
small: arteriolar disease.
generalized low arteriolar flow= watershed infarcts

12

Describe the evolution of an infarct (gross)

first several hours: no changes
1-2 days: pale and soft tissue
day 2: blurring of the grey-white junction (edema)
(peaks at day 5-7). eventually takes on a cyst like structure

13

Describe the evolution of an infarct (microscopic)

initially, loss of color
after 12 hrs, shrunken pyknotic nuclei and neurons with eosinophilic cytoplasm
at first you might see neutrophils appear, but then you get monocytes and microglia to come clean up debris. Eventually converted to foamy macrophages. Reactive astrocytes as early as 1 wk post insult. Day 10: neovascularization. 3 wks: cavitation. will continue until the infarct is a cavern filled with astrocytes and serous fluid.

14

What are the common causes of hemorrhagic infarcts? Important risk factor?

usually due to emboli, but could be other causes. usually secondary to reperfusion. of damaged tissue. Risk factor: a fib.

15

What are some characteristics of embolic hemorrhagic infarcts?

often multiple and of differing ages
often at the grey-white juntion

16

What is classic presentation of fat emboli?

(bone marrow embolization post-trauma)
widespread petechial hemorrhage of the white matter. Extensive hematoma seen in pts with on anticoagulants

17

Where and when might you see venous infarcts? Risk factors?

often hemorrhagic
seen after thrombotic occlusion of the superior saggital sinus or other veins.
Risk factors:pregnancy, oral contraceptives, coagulation disorders, dehydration, malignancy

18

What is lacunar infarction? What are predisposing conditions?

arteriorlar disease of small intraparenchymal vessels. predispostion: diabetes and HTN

19

What is the definition of a lacune?

small cavitary lesions less than 1cm in dimention

20

Where do lacunae preferentially occur?

basal ganglia, internal capsule, basis pontis, and hemispheric white matter

21

What is subcortical arteriosclerotic leukoencephalopathy?

seen in pts with HTN
multicentric degeneration of cerebral white matter with many lacunar infarcts. may present as dementia