⬅ Home
2# Vascular Diseases of CNS I
1. The most vulnerable neurons in global cerebral hypoxia are:
Motor neurons of spinal cord
Hippocampal pyramidal neurons
Brainstem nuclei
Oligodendrocytes
Explanation:
Selective vulnerability in global hypoxia affects pyramidal neurons of the hippocampus, Purkinje cells, basal ganglia neurons, and watershed cortical neurons.
2. Watershed infarcts most commonly occur at the junction between:
MCA and PCA only
ACA and PCA
Basilar and vertebral arteries
ACA and MCA
Explanation:
Watershed infarcts occur at border zones, most classically between ACA–MCA and MCA–PCA territories.
3. Red neurons appear histologically after ischemic injury at approximately:
12–24 hours
1–3 hours
3–5 days
2–3 weeks
Explanation:
Red neurons are an early ischemic change appearing after 12–24 hours.
4. Pseudo-laminar necrosis is classically seen in:
Focal embolic infarcts
Venous infarction
Global hypoxic-ischemic encephalopathy
Intracerebral hemorrhage
Explanation:
Pseudo-laminar necrosis reflects selective cortical layer vulnerability in global ischemia.
5. The most common type of cerebrovascular accident is:
Intracerebral hemorrhage
Ischemic infarction
Subarachnoid hemorrhage
Venous infarction
Explanation:
Infarctions account for approximately 80% of all strokes.
6. The artery most commonly affected by embolic infarction is:
Anterior cerebral artery
Posterior cerebral artery
Basilar artery
Middle cerebral artery
Explanation:
The middle cerebral artery is the most common site of embolic occlusion.
7. Hemorrhagic (red) infarcts are most commonly due to:
Embolic occlusion
Chronic hypertension
Watershed ischemia
Lacunar infarction
Explanation:
Embolic infarcts are often hemorrhagic due to reperfusion of necrotic tissue.
8. Gross changes in cerebral infarction typically become visible after:
6–12 hours
12–24 hours
48 hours
7 days
Explanation:
No gross changes are seen before 48 hours; infarcts become soft, swollen, and wedge-shaped afterward.
9. The correct chronological order of histologic changes in CNS infarction is:
PMNs → edema → macrophages → gliosis
Gliosis → red neurons → PMNs → macrophages
Edema → macrophages → PMNs → gliosis
Edema → red neurons → PMNs → macrophages → gliosis
Explanation:
CNS infarcts progress from edema → red neurons → neutrophils → macrophages → gliosis.
10. Macrophages peak in cerebral infarction at:
24–48 hours
7–14 days
3–5 weeks
After 2 months
Explanation:
Macrophage activity peaks between 7–14 days during infarct cleanup.
11. Wallerian degeneration refers to:
Distal axonal degeneration after infarction
Neuron death due to hypoxia
Reactive gliosis in cortex
Vascular recanalization
Explanation:
Wallerian degeneration is axonal degeneration distal to the site of injury with myelin breakdown.
12. Venous infarctions are characteristically:
Pale and unilateral
Restricted to white matter
Very hemorrhagic and bilateral
Confined to brainstem
Explanation:
Venous sinus thrombosis causes hemorrhagic, often bilateral parasagittal cortical infarcts.
13. The most common cause of primary intracerebral hemorrhage is:
Tumors
Vasculitis
Amyloid angiopathy
Hypertension
Explanation:
Chronic hypertension is the most common cause of primary intracerebral hemorrhage.
14. Charcot–Bouchard microaneurysms occur in:
Cortical arteries
Deep penetrating vessels of basal ganglia
Venous sinuses
Leptomeningeal arteries
Explanation:
These microaneurysms arise in small penetrating vessels due to chronic hypertension.
15. Lacunar infarcts are best described as:
Tiny cystic infarcts in deep grey matter
Large cortical wedge-shaped infarcts
Hemorrhagic infarcts
Venous infarcts
Explanation:
Lacunar infarcts are small cystic lesions in basal ganglia, thalamus, and pons due to HTN.
16. Cerebral amyloid angiopathy most commonly causes:
Deep hemorrhage
Venous thrombosis
Superficial lobar hemorrhage
Lacunar infarcts
Explanation:
Amyloid deposition in cortical vessels predisposes to superficial lobar hemorrhages.
17. Massive brain herniation leading to brainstem hemorrhage is called:
Charcot hemorrhage
Petechial hemorrhage
Slit hemorrhage
Duret hemorrhage
Explanation:
Duret hemorrhages occur due to downward herniation causing brainstem vessel tearing.
18. Slit hemorrhages are best explained by:
Amyloid deposition
Healing of ruptured small penetrating vessels
Venous sinus thrombosis
Embolic infarction
Explanation:
Slit hemorrhages are healed ruptures of small hypertensive vessels forming slit-like cavities.
19. Hyaline arteriolosclerosis in hypertension primarily affects:
Deep penetrating arteries
Cortical veins
Circle of Willis
Meningeal arteries
Explanation:
Hyaline arteriolosclerosis affects small deep vessels supplying basal ganglia, thalamus, and pons.
20. Which feature is characteristic of intracerebral hemorrhage pathology?
Prominent inflammatory infiltrate
Extensive neuronal necrosis
Early cavitation
Well-demarcated hematoma with edema
Explanation:
Intracerebral hemorrhage shows a well-defined hematoma with edema and minimal inflammation.