SCRN practice questions, balanced like the real exam

A fall of 3 GCS points with new vomiting on day 2 of a large infarct suggests swelling or hemorrhagic transformation; it needs urgent imaging and a decision on treatment.

Extra fluid does not treat a neurologic decline and, if hypotonic or excessive, can worsen brain swelling.

Treating the vomiting as a stomach problem masks a sign of rising intracranial pressure and loses an hour.

A deteriorating neuro exam must be reported at once; delayed reporting is a failure to rescue.

The 220/120 threshold is for the first 48 to 72 hours in patients without reperfusion therapy, not a long-term limit.

Rapid IV lowering to a low target can drop perfusion to vulnerable brain and is not needed in a stable patient.

Permissive hypertension applies only to the first 48 to 72 hours; months of untreated BP raise recurrence risk.

Once the patient is neurologically stable and past the first 48 to 72 hours, restarting home BP drugs for readings of 140/90 or higher is reasonable and begins secondary prevention.

185/110 is the pre-lytic ceiling for ischemic stroke; it is too loose a target for an active intracerebral bleed.

In spontaneous ICH with SBP 150 to 220, lowering to about 140 and holding it between 130 and 150 is reasonable to limit hematoma growth; dropping below 130 has been linked to harm.

Permissive hypertension up to 220/120 applies to ischemic stroke without reperfusion, not to hemorrhage, where high pressure drives hematoma expansion.

Very aggressive lowering risks kidney injury and cerebral hypoperfusion without extra reduction in bleeding.

An air bolus can sound gastric even when the tube sits in the lung or esophagus, so auscultation is not reliable.

The water test is outdated and unsafe: the absence of bubbles does not exclude airway placement and the patient may aspirate.

A small-bore tube can slip into the airway without a cough in a patient with impaired reflexes, so an X-ray is the standard confirmation before anything is infused.

Being able to speak does not exclude a small tube in the airway, and many patients after stroke have aphasia or dysarthria.

Oral fluids are unsafe before a swallow screen, and staying upright keeps the brain underperfused.

A new or worse deficit is never routine fatigue; it needs assessment and reporting now.

Worsening weakness on sitting up suggests orthostatic hypoperfusion of penumbral tissue; lowering the head restores flow while the nurse measures BP and the deficit.

Pushing on while the deficit worsens risks extending the infarct and a fall.

Lying flat lets secretions pool at the back of the throat and raises aspiration risk.

A patient with impaired swallowing can aspirate a mouthful of liquid; only small amounts with suction are used.

Foam swabs moisten the mouth but do not remove plaque; mechanical brushing is what lowers the bacterial load.

Brushing removes the plaque that seeds aspiration pneumonia, suction clears the fluid the patient cannot swallow, and the raised head keeps secretions out of the airway.

Choosing a texture is part of the SLP evaluation; thickened liquids can still be aspirated.

Until the SLP clears oral intake the patient stays NPO; moistening the mouth relieves thirst without delivering a swallow of liquid, and it does not replace brushing.

Ice chips melt into thin water, the texture most easily aspirated, so they are oral intake and are held after a failed screen.

A chin tuck is a strategy the SLP may prescribe after assessment; the nurse cannot assume it makes water safe.

Supporting the family's spiritual and cultural practices is part of end-of-life and palliative care; the nurse accommodates the ritual and works care around it.

Visitor limits applied rigidly at the end of life put routine ahead of the family's needs, and stimulation is not a concern here.

Spiritual support matters most during uncertainty; waiting may mean the family misses the chance.

A prayer ritual raises no ethical conflict, so an ethics referral only adds delay.

Passive motion keeps joints mobile but does not maintain strength or endurance in a patient able to move.

Two more days of bed rest add weakness, VTE and pneumonia risk without benefit.

Turning protects skin but is not mobility; waiting for PT wastes the early recovery window.

A stable patient after a mild stroke can begin protocol-based mobility under nursing care; it prevents deconditioning while the PT evaluation is pending.

Pantoprazole has little effect on CYP2C19 and is a usual choice when a PPI is needed with clopidogrel.

Omeprazole (and esomeprazole) inhibits CYP2C19, the enzyme that turns clopidogrel into its active form, and the FDA label advises against combining them.

Dexlansoprazole has not shown a meaningful reduction in clopidogrel activation and is not the PPI singled out for avoidance.

Rabeprazole is mostly cleared by non-enzymatic pathways and interacts with clopidogrel far less than omeprazole.

This is the number already compliant at 72%, not the number added.

This takes the 18-point change in percentage as a count of patients; percentage points must be applied to the 150 discharges.

This is the total compliant at 90%; the gain is the difference between the two totals.

At 72% of 150, 108 patients get compliant education; at 90% the number is 135, so the gain is 135 minus 108, or 27 patients.

Hypertension is managed by controlling BP; it is not an indication for carotid ultrasound in a person without symptoms.

No guideline recommends routine yearly carotid ultrasound by age; age alone does not justify screening.

In adults without symptoms the low prevalence of significant stenosis means screening leads to more false positives and harmful procedures than strokes prevented; USPSTF recommends against it.

Treating risk factors prevents far more strokes than imaging; an ultrasound cannot stand in for BP and lipid control.

Agitated saline injected IV shows bubbles crossing from the right to the left atrium through a patent foramen ovale, especially when the patient strains.

A prolonged monitor looks for paroxysmal atrial fibrillation, another cryptogenic stroke workup step, but it cannot detect a PFO.

CTA shows the cerebral and cervical arteries, not the interatrial septum.

Carotid ultrasound looks for stenosis in the neck arteries; it cannot show a shunt inside the heart.

A GCS of 7 with snoring respirations and vomit in the mouth means the airway is not protected; clearing and securing it comes before BP control or reversal.

BP control is urgent in ICH, but a patient aspirating vomit with an obstructed airway will deteriorate faster from hypoxia.

Warfarin reversal is time-critical but follows airway management; it can be prepared in parallel once the airway is safe.

Transporting an unprotected airway to the scanner risks aspiration and arrest, and repeat imaging does not change the immediate priority.

Asthma causes wheezing and prolonged expiration, not pink frothy sputum, and the patient has no history of it.

A massive catecholamine surge after a high-grade SAH raises pulmonary capillary pressure and permeability, causing sudden frothy pulmonary edema in someone with a healthy heart.

PE causes sudden dyspnea and hypoxia, but it does not produce frothy sputum with bilateral crackles.

Aspiration pneumonia develops over a day or more with fever and focal infiltrates, not abrupt pink frothy sputum.

Hydrocephalus would show enlarged ventricles on the CT, which is described as clear.

The sodium is normal, which excludes hyponatremia as the cause of the confusion.

New confusion and a focal deficit on days 3 to 14 after SAH, with normal sodium and no new bleed or hydrocephalus, is delayed cerebral ischemia, often from vasospasm.

The aneurysm has been coiled, and a rebleed would show new blood on CT with a sudden decline.

Gaze away from a hemispheric lesion is seen with seizures or some thalamic and pontine lesions, not a destructive MCA stroke.

Upward deviation is not a sign of hemispheric stroke; eyelid retraction suggests a dorsal midbrain lesion.

Downward and inward deviation points to thalamic or dorsal midbrain injury, not an MCA infarct.

The left frontal eye field drives gaze to the right; when it is knocked out, the intact right hemisphere pushes the eyes to the left, so they look toward the lesion.

Sudden deficit with vomiting and very high BP on an anticoagulant suggests hemorrhage, but only imaging can tell bleed from infarct; CT comes first and must not wait for labs.

Reversal before imaging risks giving a prothrombotic drug to a patient with an ischemic stroke; the diagnosis comes first.

Lab results can follow the scan; waiting for them delays both diagnosis and any treatment.

A catheter is not urgent and adds infection risk; it should not delay imaging.

A small deep infarct in a stable patient causes no dangerous swelling, so there is no indication for decompression.

Patients 60 or younger whose malignant MCA infarct swells despite medical care gain the most from decompression done within 48 hours of onset.

By day 5 the swelling has usually peaked and the evidence for benefit comes from surgery within 48 hours.

Over 60 the functional benefit of surgery is smaller and the decision rests heavily on the patient's own wishes, so this patient is not the best candidate.

No proven reversal exists for antiplatelet drugs in ICH, and transfused platelets did more harm than good.

A count of 210,000 is normal; the problem is platelet function, and the count threshold here is invented.

In the PATCH trial, platelet transfusion for antiplatelet-associated ICH in patients not having surgery increased death or dependence, so it is not recommended.

Plasma replaces clotting factors and does nothing for antiplatelet drugs; it adds volume and transfusion risk.

Moving the patient before the bolus adds transport time; the lytic is given in the CT suite or ED.

Coagulation results are not required unless a coagulopathy is suspected; waiting for them delays treatment.

Treatment can follow the treating physician's read of the images; waiting for the formal report adds minutes.

Target: Stroke encourages premixing the lytic for likely candidates so the bolus can start the moment hemorrhage is excluded; an unused dose is an accepted cost.

Surgery is done to relieve life-threatening swelling and herniation, not to prevent seizures.

Hemicraniectomy removes bone, not brain, and it does nothing to prevent a recurrent stroke.

Decompression lets the swollen brain expand outward and roughly halves mortality, but it does not restore infarcted tissue, so many survivors live with moderate to severe disability.

Dead brain does not recover after decompression; setting this expectation misleads the family's decision.

Seizures in SAH occur mostly at onset; this timing is invented and is not the reason for early treatment.

An unsecured aneurysm is most likely to rebleed in the first day, often within hours, and a rebleed is frequently fatal, so it is secured as early as possible.

Acute hydrocephalus can appear within hours of the bleed; it is not limited to late presentation.

Arterial narrowing after SAH starts around day 3 and peaks between days 3 and 14, not within hours of the rupture.

ASPECTS starts at 10 and subtracts one point per affected region; the lentiform nucleus, internal capsule and insula are three regions, so 10 minus 3 is 7.

This subtracts a fourth region, such as the caudate, which is not described as involved.

Ten means no early ischemic change, but three regions are affected.

Three is the number of affected regions, not the score; the score counts down from 10.

This total usually leaves out the age point; the ICH score adds 1 for age 80 or older.

This counts only one item; GCS, volume and age each score here.

This adds a point for intraventricular extension or an infratentorial site, and neither is present.

ICH score: GCS 5 to 12 gives 1, volume of 30 mL or more gives 1, age 80 or older gives 1, and no intraventricular or infratentorial blood adds 0, for a total of 3.

The core is small, but the mismatch ratio of about 1.4 is below 1.8, so there is too little salvageable tissue to qualify.

A 75 mL core is over the 70 mL limit, and the ratio of about 1.5 is too small, even though the penumbra looks large.

DEFUSE-3 required a core under 70 mL, a mismatch ratio of at least 1.8 and a mismatch volume of at least 15 mL; 105 over 22 is a ratio near 4.8 with 83 mL of penumbra.

The ratio of about 1.8 looks acceptable, but a 90 mL core exceeds the trial's 70 mL limit.

Early ischemia looks dark or blurred on CT; bright tissue means blood (a bright vessel sign is a clot inside an artery, not brain tissue).

BP control is a gate for ischemic stroke; it cannot make a lytic safe in a patient who is bleeding.

The first CT already shows the hemorrhage, which needs its own treatment now, not a repeat scan.

A well-defined hyperdense area in the basal ganglia at 2 hours is acute blood, a typical hypertensive hemorrhage, and any intracranial hemorrhage excludes thrombolysis.

Last known well sets eligibility for thrombolysis and thrombectomy, and the spouse may be the only person who can give it; everything else can be found later.

The first scan is a noncontrast CT, and a contrast allergy can be managed; it does not decide treatment eligibility.

Anticoagulant use matters, but a complete list takes far more than a minute and can come from the pharmacy record; the time cannot be recovered later.

A recent stroke within 3 months is a lytic consideration, but the time of onset of this event comes first.

The Norton scale predicts pressure injury risk and has nothing to do with motor impairment.

The Fugl-Meyer Assessment scores motor recovery of the upper and lower limb item by item and is the most common motor impairment outcome in rehabilitation trials.

The modified Rankin Scale grades overall disability on a 0 to 6 scale; it does not rate the arm and leg item by item.

The GCS rates level of consciousness in acute brain injury; it does not measure limb motor recovery.

Short, sudden crying that does not match mood fits pseudobulbar affect, a different condition with different treatment.

Loss of interest or pleasure is a core symptom of depression, which is common after stroke and slows recovery, so families should report it.

Being tired after a long therapy day is expected; it does not by itself suggest depression.

Speech that slows with fatigue reflects the stroke deficit, not mood.

Subluxation causes shoulder pain but does not explain the swollen, shiny, painful hand.

Arm DVT causes swelling and aching, but not shiny skin with shoulder pain; upper limb DVT is uncommon without a central line.

Central pain is a burning pain in the area of sensory loss without swelling or skin changes, usually after a thalamic stroke.

A swollen, shiny, painful hand with pain in the same shoulder weeks after a stroke is the shoulder-hand form of complex regional pain syndrome.

Small bites on the stronger, unaffected side give better control and sensation and keep food from pocketing in the weak cheek.

Food on the weak side pockets where the patient cannot feel or clear it, raising aspiration risk; exercise belongs in therapy, not meals.

Large bites are harder to control and raise the risk of choking and aspiration.

Tilting the head back opens the airway to the food; a chin-down position is the usual protective posture.

Socks protect the skin from friction and moisture; bare skin in a brace invites breakdown.

The AFO is mainly worn while walking to hold the foot up; night use does not help gait.

A new orthosis can rub, and sensation may be reduced after a stroke; redness that lasts after removal means the brace needs adjusting before a wound forms.

Fatigue is when foot drop and tripping are most likely, so this is when the brace matters most.

Dependent edema in a flaccid hand comes from lack of muscle pumping; elevation and active-assisted or passive movement help fluid return.

Ice on skin with reduced sensation risks cold injury and does not treat dependent edema.

A tight splint on a swollen hand restricts circulation and can cause skin damage.

A dependent hand fills with more fluid; it should be supported at or above heart level.

Lenticulostriate arteries branch off the occluded M1 and are end arteries, so they are cut off themselves and supply no collateral flow.

External-to-internal carotid collaterals run mainly through the ophthalmic artery and matter in ICA occlusion, not in an M1 clot beyond the circle of Willis.

Veins drain blood away from the brain; they cannot deliver arterial blood to ischemic tissue.

Pial anastomoses over the cortex let ACA and PCA blood flow backward into the MCA territory, and their strength largely sets how long the penumbra survives.

RCVS causes thunderclap headaches with segmental narrowing that resolves within weeks; it is mostly seen in adults.

Fibromuscular dysplasia gives a string-of-beads pattern in mid-cervical or renal arteries, mostly in women, not a collateral network.

Progressive narrowing of both distal internal carotids with a fine collateral network that looks like a puff of smoke on angiography is moyamoya; crying-induced hyperventilation lowers CO2 and triggers TIAs.

Vasculitis causes beading and narrowing of many medium and small vessels, often with headache and cognitive change, not symmetric distal ICA occlusion.

Abulia is lack of initiative, often after frontal damage; the patient tries to act but cannot produce the movement.

The patient understands and has the strength but cannot turn the idea into the learned movement; dominant parietal lesions classically cause ideomotor apraxia.

Visual agnosia is failure to recognize objects by sight; the patient here fails to act on a spoken command.

Receptive aphasia means the request is not understood, but this patient understands it.

Infarcts in several territories with a very high D-dimer in active adenocarcinoma point to cancer-related hypercoagulability (Trousseau syndrome), often with nonbacterial thrombotic endocarditis.

The carotids show no stenosis, and infarcts in several territories cannot come from one carotid.

Small-vessel disease causes single small deep infarcts, not multiple territorial ones.

RCVS presents with thunderclap headaches and is not tied to a high D-dimer or cancer.

Fiber crossing at the chiasm explains which half of each retina maps to each side, not why the macular cortex survives.

The retina is not injured in an occipital infarct; the visual loss is cortical.

A PCA branch would be lost along with the rest of the PCA territory, so it cannot explain why central vision survives.

The occipital pole, where central vision is mapped, often receives blood from MCA branches as well as the PCA, so central vision may survive a PCA infarct.

The calcarine cortex lies in the core of the PCA territory, not at an ACA-MCA border.

The inferior temporal lobe is supplied mainly by PCA branches and is not the ACA-MCA border zone.

The ACA and MCA territories meet along a strip near the top of the convexity beside the midline, which is where cortical watershed infarcts from low flow occur.

The pons is supplied by the basilar artery and lies outside the anterior circulation.

The cerebral peduncle carries descending motor fibers through the midbrain; it does not connect the hemispheres.

The corona radiata is the fan of projection fibers above the internal capsule within one hemisphere.

The internal capsule carries fibers between the cortex and the brainstem and spinal cord on one side, not across to the other hemisphere.

The corpus callosum is the main commissure linking the two hemispheres, and lesions of it cause disconnection signs such as alien hand.

Truncal ataxia causes unsteady sitting and swaying without a consistent push toward one side.

Actively pushing toward the weak side with the strong limbs and resisting correction to midline is pusher syndrome, a disorder of perceived body verticality.

Orthostatic hypotension causes dizziness or fainting on standing, not pushing against correction.

Neglect often coexists after right hemisphere strokes, but it causes inattention to the left, not active pushing with the strong arm.

Blood in the ventricles can block CSF outflow; rising pressure causes drowsiness, and pressure on the dorsal midbrain causes downward gaze deviation, so an EVD may be needed.

A thalamic hemorrhage is usually hypertensive, not aneurysmal; there is no aneurysm to rebleed.

Nonconvulsive seizures can lower consciousness after a hemorrhage, but they do not produce forced downward gaze with sluggish pupils; EEG would be needed, and the CT picture points to blocked CSF flow.

Hyponatremia can cause drowsiness, but it does not explain sluggish pupils and forced downward gaze on day 1.

Facial pain loss on one side is part of lateral medullary syndrome from a vertebral or PICA occlusion.

Severe dysphagia is typical of brainstem and large MCA strokes, not of a PCA infarct limited to the temporal lobe.

The PCA supplies the medial temporal lobe and hippocampus, so damage there, especially on the left, impairs the formation of new memories; teaching needs written cues and family involvement.

Leg-predominant weakness comes from an ACA stroke affecting the medial motor strip.

A right cerebellar stroke causes right-sided ataxia, but it would not weaken the right side of the face.

The speech problem is slurring, a motor articulation problem; language itself is intact, so it is not aphasia.

A cortical MCA branch infarct on the left would usually cause aphasia or other cortical signs, which are absent.

Dysarthria with facial weakness and a clumsy hand, without cortical signs, is the dysarthria-clumsy hand syndrome, a classic lacunar pattern from a small deep infarct in the pons or internal capsule.

Translation removes one barrier, but a single mailing gives no personal contact or follow-up.

A passive website in English misses both the language and access barriers of this community.

Community health workers who share the language and culture build trust, reach people where they live and follow up, which improves BP control in underserved groups.

A language the audience may not speak, in a place they may not reach, excludes the people the program is for.

The Pacific Northwest has stroke mortality near or below the national average.

The stroke belt covers southeastern states such as North Carolina, South Carolina and Georgia, where stroke mortality has long been higher than the national average.

New England has among the lowest stroke death rates in the country.

The upper Midwest is not part of the stroke belt, whose excess deaths are concentrated in the Southeast.

Warfarin is cleared by the liver; it needs INR monitoring but no renal dose adjustment.

About 80% of dabigatran is cleared by the kidneys, the most of any oral anticoagulant, so a creatinine clearance below 30 mL/min calls for a reduced dose or another agent.

Only about 27% of apixaban is cleared by the kidneys, which makes it a usual choice when kidney function is reduced.

About a third of rivaroxaban is cleared unchanged by the kidneys; it needs dose adjustment but depends on them less than dabigatran.

A survivor of a cardioembolic stroke has a high risk of another one, and modeling shows a person would have to fall very often for bleeding to outweigh that benefit, so one fall is not a reason to stop.

Stopping after one fall trades a small bleeding risk for a much higher risk of recurrent stroke; fall prevention is added instead.

Older patients have the highest stroke risk and gain the most from anticoagulation; age alone is not a contraindication.

Aspirin is far less effective than an anticoagulant for AF and still causes bleeding, so it is not a safer substitute.

Every stroke patient should be assessed by rehabilitation professionals early in the admission, so therapy and discharge planning can start while the patient is in the hospital.

Passive range of motion alone undertreats a stable patient who can begin active, assisted mobility.

Waiting for discharge loses days of early rehabilitation and leaves the discharge plan without the therapists' input.

OT and SLP are core inpatient stroke services; swallowing and self-care must be assessed before discharge.

Waiting the full infusion time before requesting transport adds an hour of avoidable delay to thrombectomy.

MRI at the sending site lengthens door-in-door-out time and does not change the decision to transfer.

Calling for transfer at the first suspicion of an LVO, rather than after treatment at the spoke is complete, removes the biggest delay in door-in-door-out time.

A repeat scan at the spoke site adds time; the receiving center reimages if needed.

Antithrombotics are held for 24 hours after any lytic, whatever the agent.

Tenecteplase is a single bolus, so there is no hour-long infusion to time, protect or stop en route; the BP and neuro monitoring after a lytic still apply.

Post-lytic neuro checks start every 15 minutes regardless of the agent; a single bolus does not relax monitoring.

The post-lytic limit of 180/105 mm Hg applies to tenecteplase just as to alteplase.

Replacing walking with a wheelchair removes practice, speeds deconditioning and deepens the fear.

Inactivity weakens the patient and reinforces avoidance; fear does not resolve without exposure.

Sedating drugs such as benzodiazepines raise fall risk and do not build confidence.

Fear of falling is reduced by safe, progressive exposure: supervised exercise that slowly increases balance demands builds both ability and confidence.

Stopping an antiplatelet after a stroke raises recurrence risk, and most dental extractions can be done while it continues, so any change is decided with the prescriber.

Ibuprofen does not give reliable antiplatelet protection and adds GI bleeding and BP effects.

Stopping on one's own for a minor procedure leaves the patient unprotected, and local measures usually control dental bleeding.

Doubling raises bleeding risk without making up for missed protection.

Nimodipine does not open narrowed arteries on angiography, yet it improves neurologic outcome after SAH; stopping it gives up that benefit.

Dose-related hypotension is managed by giving the same daily amount as 30 mg every 2 hours, which flattens the BP dip and keeps the outcome benefit of the full 21-day course.

Stretching the interval lowers the total daily dose below the regimen shown to improve outcome, and each 60 mg dose still drops the BP.

Prophylactic induced hypertension is not recommended; vasopressors are reserved for new ischemic deficits.

Short-term DAPT is for minor stroke without a surgical lesion; it does not replace or postpone revascularization of a symptomatic stenosis.

Symptomatic 70 to 99% stenosis is an indication for surgery now; waiting for a second stroke accepts preventable harm.

Recurrence risk is highest in the first days after a symptomatic carotid event, so for a nondisabling stroke with 70 to 99% stenosis endarterectomy is done early, ideally within 2 weeks.

Waiting weeks was once common for fear of bleeding into the infarct, but most preventable recurrences happen during that wait.

Neglect, slowed processing and visual field loss can persist without the patient noticing, so a structured clinical and on-road evaluation by a driving rehabilitation specialist decides when driving is safe.

Acuity and field screening miss the attention deficit of neglect; normal vision does not mean the patient will notice what happens on the left.

Self-assessment is unreliable after a right hemisphere stroke, where reduced awareness of deficits is common; confidence does not show attention to the left side.

A passenger cannot correct a missed hazard on the left in time, and short trips still expose the patient to intersections where neglect causes crashes.

The lipid result guides the dose later; it is not a reason to withdraw a drug the patient already takes.

Patients already on a statin keep taking it during the acute stroke; stopping it was linked to worse early outcomes, and it is part of the long-term plan anyway.

There is no hepatic reason to pause a statin the patient has tolerated for years, and an interruption removes its benefit at the worst time.

Fibrates do not lower stroke risk and do not replace a statin; the switch also stops the statin abruptly.

Scattered petechiae are not a hematoma that can be evacuated, and surgery would add risk to a stable patient.

Reversal is for symptomatic hemorrhage with neurologic worsening; giving it for asymptomatic petechiae adds thrombotic risk without benefit.

Petechial hemorrhagic change inside an infarct is common after reperfusion and, with a stable exam, needs no reversal; neuro checks continue so any decline is caught early.

BP after a lytic is kept below 180/105, and 150/84 already meets it; pushing it lower can drop perfusion to the penumbra.

This intensity is used for some mechanical valves, not dissection; it adds bleeding risk, and treatment is time-limited.

Healing takes time, and the early weeks carry the highest risk of embolic stroke from clot on the torn wall.

Stenting is reserved for recurrent ischemia despite medical therapy; most dissections heal on their own with antithrombotic treatment.

Trials comparing antiplatelet and anticoagulant therapy after cervical dissection found similarly low recurrence, so either kind of antithrombotic for 3 months is reasonable while the vessel wall heals.