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ABPN Vascular Neurology study materials
ABPN Vascular Neurology study resources

ABPN Vascular Neurology practice questions

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Question 1Cerebrovascular Anatomy, Physiology, and Pathophysiology

Which vessel directly connects the anterior and posterior cerebral circulations within the circle of Willis?

  1. Middle cerebral artery
  2. Superior cerebellar artery
  3. Posterior communicating artery Correct answer.
  4. Anterior communicating artery

Explanation

The posterior communicating arteries link the internal carotid system to the posterior cerebral arteries, forming the lateral connections of the circle of Willis. The anterior communicating artery instead joins the two anterior cerebral arteries. This communication allows collateral flow between the anterior and posterior circulations.

Question 2Cerebrovascular Anatomy, Physiology, and Pathophysiology

Approximately what is normal cerebral blood flow in the adult cerebral cortex?

  1. 25 mL/100 g/min
  2. 120 mL/100 g/min
  3. 10 mL/100 g/min
  4. 50 mL/100 g/min Correct answer.

Explanation

Normal adult cortical gray matter CBF is about 50 mL/100 g/min, with a usual range of roughly 45 to 60. Values near 20 indicate electrical failure, and below about 10 membrane failure and infarction supervene. White matter flow is lower than gray matter flow.

Question 3Cerebrovascular Anatomy, Physiology, and Pathophysiology

Lenticulostriate arteries, which supply the basal ganglia and internal capsule, arise most commonly from which vessel?

  1. Anterior cerebral artery
  2. Posterior cerebral artery
  3. Basilar artery
  4. Middle cerebral artery Correct answer.

Explanation

The lenticulostriate perforators arise from the M1 segment of the middle cerebral artery and supply the putamen, globus pallidus, and much of the internal capsule. Their small caliber and perpendicular origin make them vulnerable to hypertensive lipohyalinosis. Occlusion produces a lacunar syndrome rather than a cortical deficit.

Question 4Cerebrovascular Anatomy, Physiology, and Pathophysiology

Bilateral infarcts in the border zones between the anterior and middle cerebral artery territories are most characteristic of which mechanism?

  1. Global cerebral hypoperfusion Correct answer.
  2. Lipohyalinosis of lenticulostriate vessels
  3. Cortical vein thrombosis
  4. Proximal middle cerebral artery embolism

Explanation

Watershed infarcts arise where the distal fields of two arterial territories meet, so a fall in systemic perfusion pressure affects them first. Cardiac arrest, severe hypotension, or carotid occlusion can produce bilateral watershed injury. Embolic and small-vessel disease produce territorial or lacunar patterns instead.

Question 5Cerebrovascular Anatomy, Physiology, and Pathophysiology

The anterior choroidal artery, which supplies the posterior limb of the internal capsule, medial globus pallidus, and choroid plexus, arises from which artery?

  1. Middle cerebral artery
  2. Basilar artery
  3. Posterior cerebral artery
  4. Internal carotid artery Correct answer.

Explanation

The anterior choroidal artery typically arises from the supraclinoid internal carotid artery just distal to the posterior communicating artery. Its occlusion can cause contralateral hemiparesis, hemianesthesia, and hemianopia. This combination reflects involvement of the internal capsule, thalamus, and lateral geniculate body.

Question 6Cerebrovascular Anatomy, Physiology, and Pathophysiology

After acute ischemic stroke, failure of the ATP-dependent Na+/K+ pump leads to cellular swelling. This process is best termed which type of edema?

  1. Interstitial edema
  2. Cytotoxic edema Correct answer.
  3. Vasogenic edema
  4. Osmotic demyelination

Explanation

Cytotoxic edema results from energy failure, loss of ion gradients, and water movement into neurons and glia. Vasogenic edema, by contrast, reflects blood-brain barrier breakdown with protein-rich fluid in the extracellular space. The two types often coexist after large infarcts.

Question 7Cerebrovascular Anatomy, Physiology, and Pathophysiology

Cerebral perfusion pressure (CPP) is calculated by which formula?

  1. MAP minus central venous pressure
  2. MAP plus intracranial pressure
  3. MAP minus intracranial pressure Correct answer.
  4. Systolic pressure minus intracranial pressure

Explanation

CPP equals mean arterial pressure minus intracranial pressure, the driving gradient for cerebral blood flow. When ICP rises or MAP falls, CPP declines and autoregulation may be exhausted. This relationship guides blood pressure and ICP management in neurocritical care.

Question 8Cerebrovascular Anatomy, Physiology, and Pathophysiology

Most spontaneous hypertensive intracerebral hemorrhages occur in which location?

  1. Lobar white matter
  2. Putamen Correct answer.
  3. Cerebellar hemisphere
  4. Pontine tegmentum

Explanation

Hypertensive hemorrhages most often involve the putamen, followed by the thalamus, pons, and cerebellum. These sites correspond to the distribution of small penetrating arteries affected by lipohyalinosis and Charcot-Bouchard microaneurysms. Lobar hemorrhage suggests a different mechanism, such as amyloid angiopathy.

Question 9Cerebrovascular Anatomy, Physiology, and Pathophysiology

A patient with an acute brain injury is hyperventilated, lowering PaCO2 from 40 to 25 mm Hg. What is the expected immediate effect on cerebral blood flow?

  1. Falls because arterioles constrict Correct answer.
  2. No change because autoregulation is pressure-dependent
  3. Rises because oxygen delivery improves
  4. Rises because arterioles dilate

Explanation

Cerebral arterioles are highly CO2-sensitive: hypocapnia causes vasoconstriction and reduces CBF, while hypercapnia causes vasodilation and increases it. This effect is used briefly to lower ICP but can worsen ischemia if sustained. The response is mediated largely by changes in perivascular pH.

Question 10Cerebrovascular Anatomy, Physiology, and Pathophysiology

In acute ischemic stroke, which cerebral blood flow threshold best approximates the penumbra, where electrical activity ceases but membrane integrity is preserved?

  1. About 5 mL/100 g/min
  2. About 35 mL/100 g/min
  3. About 60 mL/100 g/min
  4. About 20 mL/100 g/min Correct answer.

Explanation

The ischemic penumbra is commonly defined as CBF between roughly 10 and 20 mL/100 g/min, with suppressed electrical function but preserved ionic gradients. Below about 10 mL/100 g/min, membrane failure and irreversible infarction occur. The penumbra is the target of reperfusion therapy.

Question 11Cerebrovascular Anatomy, Physiology, and Pathophysiology

During the ischemic cascade, excessive synaptic glutamate most directly produces neuronal injury by which mechanism?

  1. NMDA receptor overactivation with calcium influx Correct answer.
  2. GABA-A receptor activation with chloride influx
  3. Nitric oxide synthase inhibition
  4. Voltage-gated sodium channel blockade

Explanation

Glutamate excess overactivates NMDA and AMPA receptors, opening cation channels and allowing calcium to flood the neuron. The calcium surge activates proteases, lipases, and endonucleases that degrade the cell. This excitotoxic cascade is a key target of neuroprotection research.

Question 12Cerebrovascular Anatomy, Physiology, and Pathophysiology

A patient develops vertigo, ipsilateral facial pain and temperature loss, contralateral body pain and temperature loss, dysphagia, and ipsilateral Horner syndrome. Which artery is most likely occluded?

  1. Anterior spinal artery
  2. Anterior inferior cerebellar artery
  3. Vertebral artery Correct answer.
  4. Superior cerebellar artery

Explanation

This is lateral medullary (Wallenberg) syndrome, most often caused by occlusion of the vertebral artery or its PICA branch. The lesion involves the spinothalamic tract, spinal trigeminal nucleus, nucleus ambiguus, and descending sympathetic fibers. Dysphagia and hoarseness reflect nucleus ambiguus involvement.

Question 13Cerebrovascular Anatomy, Physiology, and Pathophysiology

Sudden hearing loss, ipsilateral facial weakness, vertigo, and contralateral loss of pain and temperature sensation most suggest infarction in which territory?

  1. Posterior inferior cerebellar artery
  2. Posterior cerebral artery
  3. Anterior spinal artery
  4. Anterior inferior cerebellar artery Correct answer.

Explanation

AICA supplies the lateral pons and inner ear, so occlusion causes lateral pontine syndrome with facial nerve involvement and hearing loss. PICA infarction affects the lateral medulla and typically spares hearing. The combination of facial palsy and deafness helps localize the lesion to AICA.

Question 14Cerebrovascular Anatomy, Physiology, and Pathophysiology

The recurrent artery of Heubner, a perforator implicated in caudate and internal capsule infarction, arises from which vessel?

  1. Posterior communicating artery
  2. Posterior cerebral artery
  3. Anterior cerebral artery Correct answer.
  4. Middle cerebral artery

Explanation

The recurrent artery of Heubner arises from the A2 segment of the anterior cerebral artery and supplies the head of the caudate, anterior limb of the internal capsule, and anterior putamen. Its occlusion can cause contralateral weakness and sometimes dysarthria. It is one of the medial lenticulostriate perforators.

Question 15Cerebrovascular Anatomy, Physiology, and Pathophysiology

A patient has dense contralateral face and arm weakness, mild leg weakness, and a nonfluent aphasia. Which arterial territory is most likely involved?

  1. Anterior cerebral artery
  2. Basilar artery
  3. Middle cerebral artery Correct answer.
  4. Posterior cerebral artery

Explanation

The MCA supplies the lateral convexity, including the motor cortex for the face and arm and, in the dominant hemisphere, Broca and Wernicke areas. ACA infarction predominantly affects the leg, while PCA infarction affects vision and memory. The face-arm predominance and aphasia strongly localize to the MCA.

Question 16Cerebrovascular Anatomy, Physiology, and Pathophysiology

A patient is awake and aware but cannot move or speak, communicating only with vertical eye movements. Which vascular lesion best explains this?

  1. Bilateral thalamic infarction
  2. Bilateral medial medullary infarction
  3. Bilateral lateral medullary infarction
  4. Ventral pontine infarction Correct answer.

Explanation

Locked-in syndrome results from a ventral pontine lesion, usually basilar artery occlusion, that interrupts corticospinal and corticobulbar tracts while sparing the reticular activating system. Vertical eye movements remain because the midbrain tectum is spared. Consciousness is preserved because the dorsal pontine tegmentum is intact.

Question 17Cerebrovascular Anatomy, Physiology, and Pathophysiology

Which location is the most common site of saccular (berry) aneurysms in the circle of Willis?

  1. Posterior communicating artery
  2. Basilar tip
  3. Middle cerebral artery bifurcation
  4. Anterior communicating artery Correct answer.

Explanation

Anterior communicating artery aneurysms are the most frequent saccular aneurysms, followed by MCA bifurcation and posterior communicating artery aneurysms. ACoA rupture classically causes subarachnoid hemorrhage with frontal lobe or intraventricular extension. Posterior communicating aneurysms may produce an ipsilateral oculomotor palsy.

Question 18Cerebrovascular Anatomy, Physiology, and Pathophysiology

Delayed cerebral ischemia from vasospasm after aneurysmal subarachnoid hemorrhage most typically occurs during which interval?

  1. Months 2 to 3
  2. Weeks 4 to 6
  3. Days 3 to 14 Correct answer.
  4. Within 6 hours

Explanation

Vasospasm generally begins 3 to 5 days after hemorrhage, peaks around days 7 to 10, and resolves over 2 to 4 weeks. It is attributed to blood breakdown products in the subarachnoid space. This timing drives monitoring with transcranial Doppler and frequent neurologic checks.

Question 19Cerebrovascular Anatomy, Physiology, and Pathophysiology

An 80-year-old normotensive patient has a spontaneous lobar hemorrhage with multiple microbleeds at the gray-white junction. Which underlying condition is most likely?

  1. Hypertensive arteriolosclerosis
  2. CADASIL
  3. Cerebral amyloid angiopathy Correct answer.
  4. Moyamoya disease

Explanation

Cerebral amyloid angiopathy deposits β-amyloid in cortical and leptomeningeal vessels, causing lobar hemorrhage and corticosubcortical microbleeds in older patients. It is associated with APOE ε4 and typically spares deep structures. The peripheral microbleed pattern distinguishes it from hypertensive small-vessel disease.

Question 20Cerebrovascular Anatomy, Physiology, and Pathophysiology

Cerebral autoregulation normally maintains relatively constant blood flow across which mean arterial pressure range in adults?

  1. 60 to 150 mm Hg Correct answer.
  2. 20 to 40 mm Hg
  3. 30 to 60 mm Hg
  4. 160 to 200 mm Hg

Explanation

In normotensive adults, autoregulation keeps CBF stable between roughly 60 and 150 mm Hg MAP through arteriolar constriction and dilation. Outside this range, flow becomes pressure-passive and the brain is vulnerable to ischemia or edema. Chronic hypertension may shift the curve upward.

Question 21Cerebrovascular Anatomy, Physiology, and Pathophysiology

A patient with severe headache and papilledema has a head CT showing a hyperdense straight sinus and a triangular area of enhancement posterior to the occipital horn. Which diagnosis is most consistent?

  1. Cerebral venous sinus thrombosis Correct answer.
  2. Cerebellar infarction
  3. Subarachnoid hemorrhage from a basilar tip aneurysm
  4. Acute hypertensive putaminal hemorrhage

Explanation

The empty delta sign is enhancement of the dural sinus wall around a nonenhancing thrombus on contrast CT. Venous sinus thrombosis classically presents with headache, papilledema, and variable venous infarction, sometimes hemorrhagic. Risk factors include pregnancy, oral contraceptives, and prothrombotic states.

Question 22Cerebrovascular Anatomy, Physiology, and Pathophysiology

Which gene mutation is responsible for CADASIL, a hereditary small-vessel disease causing recurrent lacunar strokes and white matter changes?

  1. NOTCH3 Correct answer.
  2. APP
  3. CST3
  4. COL4A1

Explanation

CADASIL is caused by NOTCH3 mutations on chromosome 19, producing granular osmiophilic material in small vessel walls. It presents with migraine, lacunar infarcts, and progressive cognitive decline, often with anterior temporal pole white matter involvement. There is no specific disease-modifying therapy.

Question 23Cerebrovascular Anatomy, Physiology, and Pathophysiology

A young patient has recurrent transient ischemic attacks and a brain angiogram showing bilateral distal internal carotid stenosis with a hazy network of lenticulostriate collaterals. What is the diagnosis?

  1. Primary angiitis of the CNS
  2. Fibromuscular dysplasia
  3. Moyamoya disease Correct answer.
  4. Reversible cerebral vasoconstriction syndrome

Explanation

Moyamoya disease is characterized by progressive stenosis of the distal internal carotid and proximal circle of Willis vessels with compensatory puff-of-smoke collaterals. It causes both ischemic and hemorrhagic strokes, especially in East Asian populations. Surgical revascularization is used for recurrent ischemia.

Question 24Cerebrovascular Anatomy, Physiology, and Pathophysiology

Which cranial nerve runs within the cavernous sinus rather than in its lateral wall?

  1. Abducens nerve (VI) Correct answer.
  2. Trochlear nerve (IV)
  3. Oculomotor nerve (III)
  4. Ophthalmic division of trigeminal (V1)

Explanation

The abducens nerve runs free within the cavernous sinus, adjacent to the internal carotid artery, while III, IV, V1, and V2 lie in the lateral dural wall. This explains the early sixth-nerve palsy in cavernous sinus thrombosis or carotid-cavernous fistula. Abducens palsy produces impaired abduction of the eye.

Question 25Cerebrovascular Anatomy, Physiology, and Pathophysiology

Occlusion of the anterior spinal artery produces which characteristic neurologic pattern?

  1. Bilateral flaccid paralysis with preserved pain
  2. Bilateral proprioception loss with preserved strength
  3. Bilateral weakness and pain/temperature loss Correct answer.
  4. Unilateral pain loss with preserved strength

Explanation

The anterior spinal artery supplies the anterior two-thirds of the cord, including the corticospinal tracts and spinothalamic tracts but sparing the dorsal columns. Anterior spinal artery syndrome therefore causes bilateral weakness and loss of pain and temperature below the lesion with preserved vibration and proprioception. It most often follows aortic surgery or profound hypotension.

Question 26Cerebrovascular Anatomy, Physiology, and Pathophysiology

Which vessel normally connects the anterior and posterior components of the circle of Willis on each side?

  1. Posterior communicating artery Correct answer.
  2. Anterior communicating artery
  3. Ophthalmic artery
  4. Recurrent artery of Heubner

Explanation

The posterior communicating artery arises from the internal carotid artery and joins the posterior cerebral artery, linking the anterior and posterior circulations. The anterior communicating artery connects the two anterior cerebral arteries, while the ophthalmic and recurrent arteries of Heubner are branches rather than communicating segments.

Question 27Cerebrovascular Anatomy, Physiology, and Pathophysiology

A patient becomes profoundly hypotensive during surgery and later has bilateral proximal arm and leg weakness that spares the face and hands. Infarction is most likely in which border zone?

  1. Between the posterior cerebral and superior cerebellar arteries
  2. Between the middle cerebral and posterior cerebral arteries
  3. Between the anterior cerebral and middle cerebral arteries Correct answer.
  4. Within the lenticulostriate perforator territory

Explanation

The anterior cerebral–middle cerebral border zone includes cortical areas controlling the proximal limbs, so hypoperfusion there produces proximal greater than distal weakness with relative sparing of the face and hands. Middle cerebral–posterior cerebral border-zone infarcts more often cause visual or higher cortical deficits, and lenticulostriate infarcts are deep perforator strokes.

Question 28Cerebrovascular Anatomy, Physiology, and Pathophysiology

Pure motor hemiparesis from a lacunar infarct is most often caused by occlusion of a perforating artery supplying which structure?

  1. Cerebellar hemisphere
  2. Posterior limb of the internal capsule Correct answer.
  3. Medial longitudinal fasciculus
  4. Occipital cortex

Explanation

Lacunar infarction in the posterior limb of the internal capsule interrupts corticospinal tract fibers and classically produces pure motor hemiparesis without aphasia, neglect, or visual field loss. Cortical, cerebellar, and brainstem tegmental lesions produce different localizing syndromes.

Question 29Cerebrovascular Anatomy, Physiology, and Pathophysiology

A patient presents with sudden coma, vertical gaze impairment, and bilateral paramedian thalamic infarcts with midbrain involvement. Occlusion of which vessel is most likely?

  1. Superior cerebellar artery
  2. Artery of Percheron Correct answer.
  3. Posterior communicating artery
  4. Anterior choroidal artery

Explanation

The artery of Percheron is a variant in which a single arterial trunk arises from one posterior cerebral artery and supplies both paramedian thalami plus the rostral midbrain. Its occlusion therefore produces bilateral thalamic infarction with altered consciousness, vertical gaze abnormalities, and memory impairment.

Question 30Cerebrovascular Anatomy, Physiology, and Pathophysiology

Which artery supplies the posterior limb of the internal capsule, globus pallidus, and lateral geniculate body, and can produce contralateral hemiplegia, hemianesthesia, and homonymous hemianopia when occluded?

  1. Lenticulostriate arteries
  2. Posterior cerebral artery
  3. Superior cerebellar artery
  4. Anterior choroidal artery Correct answer.

Explanation

The anterior choroidal artery arises from the internal carotid and supplies the posterior limb of the internal capsule, globus pallidus, and lateral geniculate body, so occlusion can cause the classic triad of hemiplegia, hemianesthesia, and homonymous hemianopia. The other arteries have different dominant territories and clinical syndromes.

Question 31Cerebrovascular Anatomy, Physiology, and Pathophysiology

Occlusion of the posterior cerebral artery at its origin most typically produces which visual field defect?

  1. Superior quadrantanopia
  2. Contralateral homonymous hemianopia with macular sparing Correct answer.
  3. Monocular visual loss
  4. Bitemporal hemianopia

Explanation

The posterior cerebral artery supplies the medial occipital cortex, and occlusion produces a contralateral homonymous hemianopia. The occipital pole, which represents the macula, often retains collateral supply from the middle cerebral artery, resulting in macular sparing.

Question 32Cerebrovascular Anatomy, Physiology, and Pathophysiology

A postpartum woman has headache, seizures, and bilateral leg-predominant weakness. Imaging shows a hyperdense superior sagittal sinus and bilateral cortical hemorrhagic infarcts. Which pattern best fits this venous infarction?

  1. Cerebellar infarcts in the PICA territory
  2. Lacunar infarcts in the lenticulostriate territory
  3. Bilateral parasagittal frontal and parietal cortical infarcts Correct answer.
  4. Bilateral paramedian thalamic infarcts

Explanation

The superior sagittal sinus drains the parasagittal cortex, so thrombosis causes venous congestion and hemorrhagic infarction near the midline, often affecting the leg motor areas and producing seizures. The other patterns correspond to specific arterial territories rather than superior sagittal sinus drainage.

Question 33Cerebrovascular Anatomy, Physiology, and Pathophysiology

In a patient with long-standing poorly controlled hypertension, how is the cerebral autoregulation curve altered, and what is the clinical implication?

  1. It shifts left, so the brain tolerates hypotension better
  2. It shifts upward only for the upper limit, with no change in the lower limit
  3. It becomes a flat line at all pressures
  4. It shifts right, so the lower limit of autoregulation occurs at a higher mean arterial pressure Correct answer.

Explanation

Chronic hypertension causes arteriolar remodeling that shifts the autoregulatory plateau to higher pressures, raising both the lower and upper limits. Consequently, a blood pressure that is normal for a nonhypertensive patient may fall below the lower limit and cause cerebral ischemia in a chronically hypertensive patient.

Question 34Cerebrovascular Anatomy, Physiology, and Pathophysiology

According to the Monro-Kellie doctrine, which component is displaced first when an acute intracranial mass expands within a closed skull?

  1. Cerebrospinal fluid and venous blood Correct answer.
  2. Skull bone
  3. Brain parenchyma
  4. Arterial blood

Explanation

The Monro-Kellie doctrine states that the total volume of brain, cerebrospinal fluid, and blood within the rigid skull is fixed. Early compensation for an expanding mass occurs by displacing cerebrospinal fluid into the spinal subarachnoid space and expressing venous blood from the cranial vault; once these reserves are exhausted, intracranial pressure rises.

Question 35Ischemic Stroke: Evaluation and Acute Management

A 68-year-old man presents with sudden right hemiparesis and aphasia that began 2 hours ago. Noncontrast head CT shows no hemorrhage, and he has no other contraindications. What is the latest time from symptom onset at which intravenous alteplase may be given under standard criteria?

  1. Up to 9 hours with imaging
  2. Up to 3 hours
  3. Up to 4.5 hours Correct answer.
  4. Up to 6 hours only

Explanation

Intravenous alteplase is approved for eligible patients treated within 4.5 hours of last known well. Treatment beyond that window is not supported by standard criteria outside research. The 3-hour window is older and not the latest accepted limit.

Question 36Ischemic Stroke: Evaluation and Acute Management

A 72-year-old woman with acute ischemic stroke is being considered for IV alteplase. Her blood pressure is 192/108 mmHg. What is the most appropriate next step?

  1. Give alteplase immediately without any BP control
  2. Lower BP to <185/110, then give alteplase Correct answer.
  3. Withhold alteplase permanently
  4. Lower BP to <140/90, then give alteplase

Explanation

Blood pressure must be reduced to ≤185/110 mmHg before IV thrombolysis. Labetalol or nicardipine can be used, and the threshold should be maintained afterward. Permanent withholding is inappropriate if BP can be controlled.

Question 37Ischemic Stroke: Evaluation and Acute Management

Which finding on noncontrast head CT is an absolute contraindication to IV thrombolysis in acute ischemic stroke?

  1. Chronic small-vessel ischemic changes
  2. Acute intracranial hemorrhage Correct answer.
  3. Cerebral atrophy
  4. Old lacunar infarct

Explanation

Acute intracranial hemorrhage on CT is an absolute contraindication to IV thrombolysis. Old infarcts, chronic white matter changes, and atrophy do not preclude treatment. CT is obtained primarily to exclude hemorrhage.

Question 38Ischemic Stroke: Evaluation and Acute Management

A 60-year-old man with acute left-sided weakness has a point-of-care glucose of 42 mg/dL. His symptoms resolve after glucose administration. What is the most appropriate interpretation?

  1. Ischemic stroke; give aspirin
  2. TIA; start dual antiplatelet
  3. Stroke mimic; no thrombolysis Correct answer.
  4. Ischemic stroke; proceed with alteplase

Explanation

Hypoglycemia is a common stroke mimic, and symptoms that resolve with glucose correction do not warrant thrombolysis. Glucose should be checked in all suspected stroke patients before reperfusion decisions. Dual antiplatelet therapy is not indicated for a hypoglycemic mimic.

Question 39Ischemic Stroke: Evaluation and Acute Management

In a patient who receives IV alteplase for acute ischemic stroke, when should aspirin or another antiplatelet generally be started?

  1. Immediately after the infusion is completed
  2. After 7 days
  3. After 24 hours with repeat imaging Correct answer.
  4. After 12 hours

Explanation

Antiplatelet therapy is generally delayed for 24 hours after IV thrombolysis and started after follow-up imaging excludes hemorrhagic transformation. Early antiplatelet use increases the risk of symptomatic intracranial hemorrhage. Seven days is unnecessarily long in most patients.

Question 40Ischemic Stroke: Evaluation and Acute Management

A 65-year-old woman with acute ischemic stroke is not receiving reperfusion therapy. Her blood pressure is 210/110 mmHg and she is otherwise stable. What is the recommended approach?

  1. Lower BP to <140/90
  2. Observe unless BP exceeds 220/120 Correct answer.
  3. Give no treatment under any circumstances
  4. Lower BP to <185/110

Explanation

Permissive hypertension is allowed in acute ischemic stroke patients who are not reperfusion candidates, generally up to 220/120 mmHg. Treatment is reserved for pressures above that threshold or for specific comorbid indications. Aggressive lowering can compromise penumbral blood flow.

Question 41Ischemic Stroke: Evaluation and Acute Management

Before giving oral medications or food to a patient with acute stroke, what should be done?

  1. Wait 72 hours before any oral intake
  2. Perform a bedside swallow screen Correct answer.
  3. Give only clear liquids
  4. Obtain an MRI of the brain

Explanation

Dysphagia is common after stroke, and a bedside swallow screen should be completed before any oral intake to reduce aspiration risk. Clear liquids are not safe until swallowing is assessed. MRI does not replace a swallow evaluation.

Question 42Ischemic Stroke: Evaluation and Acute Management

A 70-year-old man with acute ischemic stroke is admitted. His LDL is 150 mg/dL. When should high-intensity statin therapy generally be started?

  1. Only after discharge
  2. Only if carotid stenosis is present
  3. After 6 months
  4. During hospitalization Correct answer.

Explanation

High-intensity statin therapy should be initiated during hospitalization for acute ischemic stroke unless contraindicated. It lowers recurrent stroke and cardiovascular risk. Waiting for discharge or carotid imaging is not necessary.

Question 43Ischemic Stroke: Evaluation and Acute Management

What is the standard intravenous dose of tenecteplase for acute ischemic stroke?

  1. 0.9 mg/kg (max 90 mg), same as alteplase
  2. 0.25 mg/kg (max 25 mg) Correct answer.
  3. 0.5 mg/kg (max 50 mg)
  4. 1.0 mg/kg (max 100 mg)

Explanation

Tenecteplase is used at 0.25 mg/kg, with a maximum of 25 mg, for acute ischemic stroke. Alteplase is dosed at 0.9 mg/kg to a maximum of 90 mg. Higher tenecteplase doses are not standard for stroke.

Question 44Ischemic Stroke: Evaluation and Acute Management

A patient with acute ischemic stroke has a platelet count of 80,000/µL. How does this affect IV thrombolysis?

  1. It requires platelet transfusion first
  2. No effect on thrombolysis
  3. It is a contraindication Correct answer.
  4. It requires half-dose alteplase

Explanation

A platelet count below 100,000/µL is a contraindication to IV thrombolysis because of bleeding risk. Platelet transfusion is not routinely recommended solely to enable thrombolysis. Half-dose alteplase is not an accepted strategy for thrombocytopenia.

Question 45Ischemic Stroke: Evaluation and Acute Management

A patient taking warfarin for atrial fibrillation presents with acute ischemic stroke. His INR is 1.9. What is correct regarding IV alteplase?

  1. Give full-dose alteplase without delay
  2. Give half-dose alteplase
  3. Do not give intravenous alteplase Correct answer.
  4. Give alteplase after vitamin K reversal

Explanation

An INR above 1.7 is a contraindication to IV alteplase, so thrombolysis should not be given. Mechanical thrombectomy may still be considered if the patient has a large vessel occlusion. Vitamin K reversal is not a standard strategy solely to enable alteplase.

Question 46Ischemic Stroke: Evaluation and Acute Management

A patient with atrial fibrillation took apixaban 6 hours ago and now has acute ischemic stroke. What is most appropriate regarding IV thrombolysis?

  1. Give intravenous tenecteplase
  2. Give intravenous alteplase
  3. Check anti-Xa level and give if low
  4. Do not give thrombolysis Correct answer.

Explanation

Recent direct oral anticoagulant use within 48 hours generally contraindicates IV thrombolysis unless reversal or a reliable assay shows minimal effect. Apixaban taken 6 hours ago is still expected to have significant anticoagulant activity. Endovascular thrombectomy can be considered independently.

Question 47Ischemic Stroke: Evaluation and Acute Management

A patient with minor ischemic stroke (NIHSS 3) and no high-risk features is started on dual antiplatelet therapy. How long should DAPT generally continue?

  1. 1 year
  2. 21 days Correct answer.
  3. 3 months
  4. 6 months

Explanation

Dual antiplatelet therapy is recommended for 21 days after minor ischemic stroke or high-risk TIA, followed by single antiplatelet therapy. This approach is based on trials showing reduced recurrent stroke with acceptable bleeding. Longer dual therapy increases bleeding without clear benefit.

Question 48Ischemic Stroke: Evaluation and Acute Management

A 75-year-old woman with MCA occlusion has a CT perfusion showing a small core and large penumbra. She was last known well 12 hours ago. What is the most appropriate treatment?

  1. Intravenous alteplase alone
  2. Aspirin alone
  3. Observation
  4. Endovascular thrombectomy Correct answer.

Explanation

Endovascular thrombectomy is beneficial up to 24 hours in selected patients with large vessel occlusion and favorable imaging. At 12 hours, IV alteplase is outside the standard window. Aspirin alone or observation would forgo proven reperfusion benefit.

Question 49Ischemic Stroke: Evaluation and Acute Management

A noncontrast CT in a patient with MCA stroke shows hypodensity in the insula, M2, M3, and caudate. What is the ASPECTS score?

  1. ASPECTS 6 Correct answer.
  2. ASPECTS 8
  3. ASPECTS 4 (large core)
  4. ASPECTS 9

Explanation

ASPECTS starts at 10 and subtracts 1 point for each affected region. Four involved regions produce a score of 6. Lower scores indicate a larger infarct and worse prognosis.

Question 50Ischemic Stroke: Evaluation and Acute Management

In acute ischemic stroke, what does a CT perfusion mismatch ratio of 2.0 with core 30 mL and penumbra 90 mL suggest?

  1. Hemorrhagic transformation
  2. Large completed infarct involving the entire territory
  3. No salvageable brain tissue at all
  4. Small core with salvageable penumbra Correct answer.

Explanation

A mismatch ratio of 2.0 with a 30-mL core and 90-mL penumbra indicates a small core with substantial salvageable tissue. This pattern favors reperfusion therapy. Hemorrhagic transformation is assessed on noncontrast CT or susceptibility imaging, not perfusion mismatch.