SCRN Anatomy, Physiology, and Pathophysiology of Stroke 5 — Questions and Answers
Question 1: Which pathological process is responsible for the 'no-reflow' phenomenon seen after cerebral ischemia-reperfusion?
- Persistent arterial vasospasm in large vessels
- Microvascular obstruction by activated leukocytes, platelets, and edematous endothelium (Correct answer)
- Re-occlusion of the previously occluded artery by fresh thrombus
- Hyperperfusion syndrome causing arteriolar dilation
Correct answer: Microvascular obstruction by activated leukocytes, platelets, and edematous endothelium
No-reflow results from microvascular obstruction by adherent leukocytes and platelets, endothelial swelling, and perivascular edema preventing restoration of perfusion despite large vessel recanalization.
Question 2: A patient with a posterior cerebral artery stroke is most likely to present with which primary deficit?
- Contralateral arm and face weakness
- Contralateral homonymous hemianopia (Correct answer)
- Ipsilateral facial palsy with contralateral hemiplegia
- Global aphasia
Correct answer: Contralateral homonymous hemianopia
The PCA supplies the occipital lobe (primary visual cortex); PCA stroke classically causes contralateral homonymous hemianopia, often with macular sparing.
Question 3: Spreading cortical depolarization in stroke contributes to infarct expansion primarily by:
- Causing immediate neuronal apoptosis in the penumbra
- Repeatedly increasing metabolic demand in vulnerable penumbral tissue, expanding the infarct core (Correct answer)
- Triggering systemic inflammatory cascades that worsen edema
- Directly rupturing blood vessels through mechanical stress
Correct answer: Repeatedly increasing metabolic demand in vulnerable penumbral tissue, expanding the infarct core
Peri-infarct spreading depolarizations repeatedly depolarize penumbral neurons, consuming limited energy reserves and progressively converting penumbra to infarct core.
Question 4: Which area of the internal capsule carries fibers controlling contralateral upper extremity movement?
- Anterior limb
- Genu
- Posterior limb (posterior one-third) (Correct answer)
- Retrolenticular limb
Correct answer: Posterior limb (posterior one-third)
Corticospinal fibers controlling the contralateral arm travel in the posterior limb of the internal capsule; the face is at the genu and the leg is most posterior.
Question 5: In hemorrhagic stroke, perihematomal edema begins to develop most significantly at what time after the initial bleed?
- Immediately (within 1 hour)
- 24–72 hours (Correct answer)
- 5–7 days
- 2–3 weeks
Correct answer: 24–72 hours
Perihematomal edema begins within hours but reaches its peak at 24–72 hours after ICH, driven by coagulation cascade activation, thrombin production, and BBB disruption.
Question 6: A stroke patient has loss of pain and temperature sensation on the right side of the face and left side of the body. This crossed sensory pattern localizes the lesion to the:
- Right thalamus
- Right lateral medulla (Correct answer)
- Left pons
- Left internal capsule
Correct answer: Right lateral medulla
In the lateral medulla, the ipsilateral trigeminal nucleus (face sensation) and the contralateral spinothalamic tract (body sensation) are adjacent; lateral medullary infarct produces crossed hemianesthesia.
Question 7: Which cerebrovascular condition is characterized by thickening of small artery walls due to hyaline material replacing smooth muscle, predisposing to both ischemic lacunar strokes and intracerebral hemorrhage?
- Cerebral amyloid angiopathy
- Lipohyalinosis (Correct answer)
- Fibromuscular dysplasia
- Moyamoya disease
Correct answer: Lipohyalinosis
Lipohyalinosis is chronic hypertension-induced degeneration of small penetrating arteries (< 400 µm), replacing smooth muscle with lipid-laden macrophages and hyaline, causing both lacunar infarcts and ICH.
SCRN Anatomy, Physiology, and Pathophysiology of Stroke 5
Which pathological process is responsible for the 'no-reflow' phenomenon seen after cerebral ischemia-reperfusion?