Neuropathology III

Question 1

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

Answer 1

from middle cerebral arteries

supply striatum and posterior limb of the internal capsule. this is an “end” artery

Question 2

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

Answer 2

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.

Question 3

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

Answer 3

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

Question 4

What is subclavian steal syndrome?

Answer 4

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)

Question 5

Where are emboli most common?

Answer 5

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

Question 6

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

Answer 6

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

Question 7

To what conditions might cholesterol emboli be secondary?

Answer 7

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

Question 8

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

Answer 8

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.

Question 9

What is the ischemic cascade that leads to damage?

Answer 9

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.
5. Ca causes glutamate release
6. Glutamate interacts with NMDA receptors and makes them more excitable.
7. Excitotoxicity leads to the release of free radicales, proteases, and more glutamate
8. all of this causes cell destruction (membrane breakdown, mitochondrial damage and apoptosis). Inflammatory response beigns

Question 10

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

Answer 10

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

Question 11

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

Answer 11

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

Question 12

Describe the evolution of an infarct (gross)

Answer 12

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

Question 13

Describe the evolution of an infarct (microscopic)

Answer 13

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.

Question 14

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

Answer 14

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

Question 15

What are some characteristics of embolic hemorrhagic infarcts?

Answer 15

often multiple and of differing ages

often at the grey-white juntion

Question 16

What is classic presentation of fat emboli?

Answer 16

(bone marrow embolization post-trauma)

widespread petechial hemorrhage of the white matter. Extensive hematoma seen in pts with on anticoagulants

Question 17

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

Answer 17

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

Question 18

What is lacunar infarction? What are predisposing conditions?

Answer 18

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

Question 19

What is the definition of a lacune?

Answer 19

small cavitary lesions less than 1cm in dimention

Question 20

Where do lacunae preferentially occur?

Answer 20

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

Question 21

What is subcortical arteriosclerotic leukoencephalopathy?

Answer 21

seen in pts with HTN

multicentric degeneration of cerebral white matter with many lacunar infarcts. may present as dementia